INFLAMMATORY CYTOKINE PROFILE IN ACINETOBACTER BAUMANNII INFECTION AND ANTIMICROBIAL RESISTANCE PATTERNS AND CLINICAL OUTCOMES IN NAJAF, IRAQ

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INFLAMMATORY CYTOKINES AND RESISTANCE PATTERNS IN ACINETOBACTER BAUMANNII INFECTION IN NAJAF, IRAQ

 

Abstract:

         The rise of multidrug-resistant Acinetobacter baumannii and its virulence to elicit a strong inflammatory response in infected patients make it one of the most important healthcare-associated pathogens. This study is a case-control study that aimed to assess the levels of the cytokine’s interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interleukin-10 (IL-10) in the serum of patients with proven A. baumannii infection, and to evaluate the relationship of these cytokines with demographic, clinical, and antimicrobial resistance traits. One hundred patients with known infection and 100 seemingly healthy controls were recruited. Conventional microbiological methods were employed for processing the clinical specimens which were finally confirmed using the VITEK 2 Compact system. ELISA was used to determine the serum concentration of cytokines. Most of the isolates were considered to be extensively drug-resistant (XDR) (77%), multidrug-resistant (MDR) (20%), and pandrug-resistant (PDR) (3%). Patients had significantly elevated levels of IL-6, TNF-α and IL-10 in their serum (p = 0.0001 for all). There was a significant correlation between the level of IL-6 and IL-10 (p = 0.019), while no correlation was found between IL-6 and TNF-α (p = 0.856) and between TNF-α and IL-10 (p = 0.284). There were no significant differences in levels of cytokines in relation to sex, age, hospitalization status, the type of hospital admission or the source of the specimen (p > 0.05). But, higher levels of IL-6 and TNF-α were significantly associated with ICU admission (p = 0.012 and 0.034, respectively) and there was no difference in IL-10 (p = 0.121). Further, significantly higher levels of IL-6, TNF-a and IL-10 were present in patients with XDR isolates than in patients with MDR isolates (p = 0.018, p = 0.027 and p = 0.025 respectively). The results indicate that A. baumannii infection is accompanied by a strong inflammatory response and immunoregulatory response, especially in the most severely ill patients and infections with highly-resistant isolates, suggesting a potential role of inflammatory cytokines as markers of infection severity and host immune activation.

Keywords: Acinetobacter baumannii, cytokine, IL-6, TNF-α, IL-10, ELISA, ICU, XDR, MDR, PDR

 

1.Introduction

          Its unique capacity to survive under extreme environment, persist in the hospital for a long time and easily develop multi-antimicrobial resistance has made Acinetobacter baumannii as one of the most troublesome opportunistic bacterial pathogens in modern healthcare systems. In recent years, the emergence of multidrug-resistant and carbapenem-resistant A. baumannii has posed significant therapeutic and epidemiological issues, especially in hospitalized and critically ill patients elsewhere. In such a scenario, the World Health Organization still considers A. baumannii as one of the critical-priority bacterial pathogens to be monitored and new therapeutic strategies to be developed, due to the limited treatment options and the growing number of healthcare-associated infections with this bacterium [18, 20]. A. baumannii is a Gram-negative coccobacillus with a strong association with hospital settings, particularly intensive care units (ICUs) and other high-risk clinical care settings. In addition to antimicrobial resistance, its clinical significance is due to virulence properties that contribute to persistence in the environment, formation of biofilms, colonization of media and devices and immune evasion of the host. These properties enable it to produce serious infections like ventilator- associated pneumonia, bloodstream infections, wound and burn infections, urinary tract infections, meningitis and sepsis. Resistant A. baumannii strains are often linked to complex treatment, poor patient outcome, and extended hospital stays, especially in susceptible patients exposed to invasive procedures or broad-spectrum antibiotics [5, 7, 18]. As the antimicrobial resistance crisis has been expanding, increasing evidence suggests that the severity of A. baumannii infection is closely related to the nature of the host inflammatory response. Following infection, A. baumannii activates innate immune pathways that stimulate the production of several inflammatory mediators, especially interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), which are central to the activation of leukocytes, endothelial stimulation, acute phase responses, and amplification of systemic inflammation. But, the overproduction and/or over-regulation of these cytokines can lead to damage of tissues and serious inflammatory complications. By contrast, interleukin-10 (IL-10) is a key anti-inflammatory cytokine involved in regulating the balance and curbing excessive inflammatory damage. Thus, measurement of both cytokines (IL-6, TNF-α) and anti-inflammatory (IL-10) may offer a better insight into the immunological response to infection with A. baumannii than the measurement of a single cytokine alone [7, 12].

           Experimental and clinical research has highlighted recent years the biological relevance of the regulation of cytokines in A. baumannii infection. High levels of IL-6 and TNF-α in serum have been linked to hyper-inflammatory response and to the progression of infection, while IL-10 seems to be involved in immune compensation and in the regulation and modulation of anti-bacterial function of macrophages. These observations indicate that inflammatory cytokines could possibly serve as useful markers of the severity of infection, but also of the nature of the host-pathogen interaction and disease progression. But the immunological response to A. baumannii infection in Iraqi patients and its correlation with clinical characteristics and antimicrobial resistance phenotypes is still not well described. Furthermore, there is a lack of studies assessing inflammatory cytokine profile in patients with proven A. baumannii infection in Iraq, especially in Najaf Province, where the rising antimicrobial resistance and healthcare-associated infections are significant clinical concerns. Most investigations available in the area so far have been mainly microbiological or antimicrobial susceptibility without considering the host inflammatory response and its association with the demographic-clinical characteristics of infected patients [1, 2, 3]. The rising of resistant A. baumannii isolates in Iraqi hospitals in conjunction with the lack of integrated immunological and clinical data, necessitated the need for integrated (immunological and clinical) studies from this country to improve understanding of the inflammatory response to this pathogen. These data could help in understanding the severity of infection, in infection-control measures, and in the provision of valuable data for future clinical applications using biomarkers. Thus, the current study was conducted to compare the serum level of IL-6, TNF-α, and IL-10 between A. baumannii confirmed infected patients and non-infected healthy people and to explore the correlation of serum level of these cytokines with the demographic parameters and clinical characteristics. The study also set out to establish the antimicrobial resistance phenotype profile of the isolated strains. In the current study, combining microbiological, clinical and immunological results, locally relevant evidence is aimed to be provided to understand the host inflammatory response to A. baumannii infection in Najaf, Iraq.

2. Material and methods

2.1 Study population and design:

          It was a case-control study to assess the serum levels of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF- α) and interleukin-10 (IL-10) among confirmed cases of Acinetobacter baumannii infection and healthy controls and correlate these with the demographic, clinical and antimicrobial resistance characteristics. The study was carried out on patients who visited or were admitted to many hospitals in Najaf Province in Iraq, during the period from October 2025 to April 2026. In total, 471 clinical specimens were taken in the first instance from patients who had indications of an infection. An example of these would be burn swabs, wound swabs, blood, sputum, urine, nasal swabs and throat swabs. All samples were taken under strict aseptic conditions and sent immediately to the Microbiology Laboratory, Faculty of Science, Kufa University and Al-Ameen Center for Advanced Research and Biotechnology for further processing. All the venous blood samples were simultaneously taken at the time of clinical sampling and stored for immunological analysis. After the microbiological processing and confirmation, 100 patients with Acinetobacter baumannii infection were recruited in the study. Concurrently, 100 apparently healthy individuals were recruited as control group to enable appropriate statistical comparison of the level of serum cytokines in infected and non-infected populations. Besides immunological evaluation, detailed demographic and clinical data were obtained from all subjects such as sex distribution, age groups, hospital of admission, hospitalization status, intensive care unit (ICU) admission and source of clinical specimens. Moreover, the antimicrobial resistance profiles of the isolated strains of A. baumannii were grouped into multidrug-resistant (MDR), extensively drug-resistant (XDR), and pandrug-resistant (PDR) to allow correlation with the immunological findings .

 

2.2 Isolation and Identification of Acinetobacter baumannii

        The isolation and identification of Acinetobacter baumannii was carried out, as outlined below. Bum swabs, wound swabs, blood, sputum, urine, nasal swabs and throat swabs were collected from the clinical setting and placed on blood agar, MacConkey agar and CHROMagar media and incubated at 37°C aerobically for 24 hours. The non-lactose fermenting colonies were then picked and further identified. The gram stain showed gram negative coccobacilli that were single or in pairs. Identification was made by biochemical tests including oxidase, catalase, triple sugar iron, oxidation-fermentation, SIM and growth at 44°C. Typical characteristics of A. baumannii, such as oxidase-negative, catalase-positive, non-fermentative metabolism, non-motility, and growth at high temperatures were confirmed in the isolates. Isolates were confirmed in the VITEK 2 Compact system (bioMérieux, France) [15]. Only confirmed A. baumannii isolates were used for further analysis.

2.3 Serum sample collection and measurement

        It carried out with the utmost care. All participants had venous blood samples taken in an aseptic manner. Samples were left to clot at room temperature and then spun at 3000 revs/min for 10 minutes. Serum was separated carefully, and stored at -20°C until the cytokines were analyzed to prevent degradation of analytes. Interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and interleukin 10 (IL-10) were determined by enzyme-linked immunosorbent assay (ELISA) kit provided by BT LAB, China as per the manufacturer's instructions. Each assay was run twice to ensure reliability and reproducibility. The optical density was determined in a microplate reader at a wavelength of 450 nm and concentrations of the cytokines were determined by standard calibration curve obtained by regression analysis. The ELISA kits for the quantification of cytokines are supplied by BT LAB, China which includes the following cytokines: human IL-6, IL-10 and the human TNF-α detection kits. These kits were used according to standardized protocols from the manufacturer for quantitative measurement of the serum concentrations of cytokines [10].

2.4. Statistical Analysis

       Data was analysed using SPSS Version 26. Mean ± standard deviation was used for continuous variables, and frequencies and percentages were used for categorical variables. The Shapiro-Wilk test was used to determine normality of data distribution. Independent samples t-tests or non-parametric equivalent tests were used for group comparisons as appropriate. Pearson or Spearman correlation analysis was performed to evaluate the correlation between serum cytokine concentrations and demographic and clinical data, as appropriate to the distribution of the data. Statistically significance was set at a p-value of < 0.05.

3.Results

            Demographic and clinical characteristics: The mean age of the patients was 36.93 ± 17.72 years. The highest frequency was observed in the 41–60 years age group (39%), followed by 21–40 years (31%), 1–20 years (24%), and >60 years (6%). There were 59% male and 41% female cases. Just over half the patients were outpatients (51%) and inpatients (49%). The number of patients admitted to the ICU was 17% and 83% of patients were non-ICU patients. As far as antimicrobial resistance patterns are concerned, most of the isolates (77%) were extensively drug-resistant (XDR), 20% were multidrug-resistant (MDR) and 3% were pandrug-resistant (PDR) which means that most of the studied isolates belonged to highly resistant strains. In addition, the study revealed that levels of cytokines were significantly higher in patients with A. baumannii infection than in healthy controls These results are summarized in Table 1.

 

TABLE 1. DEMOGRAPHIC AND CLINICAL CHARACTERISTICS OF PATIENTS WITH A. BAUMANNII ISOLATES (N=100)

Variable	Categories	N.(%) or Mean+SD
Age (year)	36.93+ 17.72
Age groups	1-20	24 (24%)
	21-40	31 (31%)
	41-60	39 (39%)
	≥61	6 (6.0%)
Sex	Male	59 (59%)
	Female	41(41%)
Hospitalization status	Inpatient	49 (49%)
	outpatient	51 (51%)
ICU admission	ICU	17(17%)
	No-ICU	83(83%)
Antimicrobial resistance phenotypes	XDR	77 (77%)
	MDR	20 (20%)
	PDR	3 (3%)

           The difference between the mean serum level of IL-6 in patients (69.79 ± 10.20 pg/mL) and the mean serum level of IL-6 in controls (16.28 ± 3.36 pg/mL) was highly significant (p = 0.0001). Similarly, TNF-α levels were significantly elevated in patients (20.14 ± 2.23 pg/mL) compared to controls (5.15 ± 2.23 pg/mL) (p = 0.0001). Also, IL-10 levels were also significantly increased in patients (16.04 ± 4.34 pg/mL) compared with controls (6.26 ± 2.06 pg/mL) (p = 0.0001) as shown in table 2.

TABLE 2. COMPARISON OF SERUM IL-6, TNF-α, AND IL-10 LEVELS BETWEEN PATIENTS WITH A. BAUMANNII INFECTION AND HEALTHY CONTROLS

Cytokines	Mean+ SD Patients (n=100)	Mean+ SD Control (n=100)	p. value
IL-6	69.79+ 10.20	16.28+ 3.36	0.0001*
TNF-α	20.74+ 4.81	5.15+ 2.23	0.0001*
IL-10	16.04+ 4.34	6.26+ 2.06	0.0001*

Furthermore, all cytokines showed a significant positive correlation with each other, except for the correlation between the level of IL-6 and IL-10 (r=0.234, p = 0.019), in contrast, no significant correlation was observed between IL-6 and TNF-α (r = -0.018, p = 0.856), nor between TNF-α and IL-10 (r=0.108, p = 0.284). (Table 3).

TABLE 3. SPEARMAN CORRELATION ANALYSIS OF SERUM IL-6, TNF-α, AND IL-10 LEVELS AMONG PATIENTS WITH A. BAUMANNII INFECTION

Cytokine		IL-6	TNF-α	IL-10
IL6	Correlation Coefficient	1.000	-0.018-	0.234
	p.value	-	0.856	0.019*
TNF-α	Correlation Coefficient	-.018-	1.000	0.108
	p.value	0.856	-	0.284
IL10	Correlation Coefficient	0.234	0.108	1.000
	p.value	0.019*	0.284	-

         There was no significant correlation between serum cytokine concentrations and the demographic or clinical characteristics (Table 4) and all were not significant (p>0.05) for both IL-6, TNF-α and IL-10 levels. However, ICU admission showed a significant association with IL-6 and TNF-α levels, where ICU patients had higher IL-6 (75.70 ± 11.98 pg/ml vs. 68.59 ± 10.12 pg/ml; p = 0.012) and higher TNF-α levels (22.64 ± 7.59 pg/ml vs. 19.90 ± 4.03 pg/mL; p = 0.034), while IL-10 showed no significant difference (p = 0.121). Finally, those Patients with XDR isolates had significantly higher levels of IL-6, TNF-α and IL-10 than those with MDR isolates (p = 0.018, p = 0.027 and p = 0.025, respectively).

 

TABLE 4. ASSOCIATION BETWEEN SERUM IL-6, TNF-α, AND IL-10 LEVELS AND DEMOGRAPHIC AND CLINICAL CHARACTERISTICS IN PATIENTS WITH A. BAUMANNII INFECTION (N=100)

IL-10 Mean+ SD	TNF-α Mean+ S	IL-6 Mean+ SD	Variable
16.38+4.48	21.15+4.80	69.61+11.08	Male	Sex
16.14+4.69	20.14+4.84	70.04+8.92	Female
0.794	0.307	0.834	p. value
14.50+ 3.76	19.51+ 3.89	68.50+ 13.30	1-20	Age group (year)
16.96+ 5.16	17.33+6.88	68.46+ 10.64	21-40
19.33+ 5.71	21.35+ 5.93	69.87+ 11.63	41-60
16.28+ 4.13	21.25+ 3.95	71.67+ 9.81	≥61
0.071	0.135	0.655	p. value
16.64+4.16	19.58+3.84	67.14+8.83	Al-Sader	Hospital
16.06+5.41	18.80+5.87	74.06+11.96	Al-Forat
16.73+4.91	21.31+4.64	67.36+11.34	Al-Najaf
16.25+5.70	20.83+7.01	74.58+9.50	Al-Hakeem
15.25+3.82	21.70+4.30	70.55+11.66	Al-Zahra
0.843	0.321	0.092	p. value
16.59+4.75	20.95+ 477	71.53+ 9.84	Inpatient	Hospitalization
15.94+429	20.52+4.89	68.11+10.37	Outpatient
0.474	0.658	0.095	p. value
17.82+ 5.91	22.64+759	75.70+ 11.98	ICU	ICU
15.92+ 4.23	19.90+ 4.03	68.59+10.12	No-ICU
0.121	0.034 *	0.012 *	p. value
17.23+4.45	19.31+4.86	68.39+10.17	Burn	Specimen source
13.66+2.54	21.33+2.95	70.66+10.57	Wound
13.90+2.92	19.80+4.87	67.30+1.69	Blood
15.87+4.27	21.62+4.73	68.68+10.72	Sputum
15.80+4.82	20.50+5.08	69.50+8.88	Urine
19.00+5.91	23.28+7.06	77.28+11.49	Nasal
16.30+5.96	19.90+4.70	73.70+11.87	Throat
0.123	0.442	0.411	p. value
17.10+4.81	20.92+4.80	71.05+10.23	XDR	Distribution of MDR, XDR, PDR
13.90+4.50	18.35+4.52	63.55+9.82	MDR
14.66+3.51	15.66+4.93	69.00+17.32	PDR
0.025 *	0.027 *	0.018 *	p. value

 

 

 

4.Discussion

           The present study found that most of the patients with Acinetobacter baumannii infection were in the age group 41-60 years with male accounting for more than female. These findings are in line with the well-established epidemiology of A. baumannii as an opportunistic healthcare associated pathogen that is mainly associated with adult patients who have been exposed to hospitalization, invasive procedures, prolonged antimicrobial therapy or underlying comorbidities [3, 4, 17]. Non-ICU cases slightly outnumbered the number of cases in the ICU for the present study. Although it is traditionally considered to be an ICU-associated pathogen, there is now evidence that A. baumannii's spread is not limited to intensive care units, and may spread to general wards because of environmental persistence and increased antimicrobial selection pressure [6, 11]. However, ICU-associated isolates still play a role as epidemiologically important isolates since critically ill patients are still a large reservoir for multidrug-resistant strains [11, 16]. However, the antimicrobial resistance analysis in the present study showed that XDR isolates were the predominant phenotype of the isolates studied in this study, MDR isolates were less common, and PDR isolates were rare. This is consistent with a recent study that revealed the emergence and dissemination of super-resistant A. baumannii strains in the hospital setting, especially in seriously ill patients and in healthcare settings that are highly exposed to antibiotics [18]. The high predominance of XDR isolates in the present study further emphasizes the clinical importance of this pathogen as well as the therapeutic problem in the local context.

         Moreover, the patients with A. baumannii infection in the current study had significantly higher serum levels of IL-6, TNF-α and IL-10 than healthy controls. These results suggest that infection with A. baumannii triggers a systemic inflammatory response with simultaneous activation of pro and anti-inflammatory pathways, the high level of IL-6 found in the present study likely reflecting activation of the acute inflammatory phase as IL-6 is a mediator of fever, acute-phase protein production, activation of leukocytes and systemic inflammation. Similarly, significant upregulation of IL-6 has been shown in experimental and clinical studies of A. baumannii infection [7, 14, 19]. Similarly, the marked increase in the levels of TNF- α indicates that innate immune activation is increased, as TNF- α is one of the first cytokines produced on encountering bacteria and plays a role in endothelial activation and inflammatory cascades. This is similar to previous studies of A. baumannii [7, 19]. The marked elevation of IL-10, however, indicates that there is a compensatory anti-inflammatory response along with the inflammatory response. IL-10 is an important immunoregulatory molecule that keeps excessive tissue damage in check and regulates macrophage mediated inflammation. Previous experimental evidence has shown that IL-10 plays a role in modulation of inflammatory signaling pathways and immune regulation and host protection during A. baumannii infection [12, 9, 21]. Thus, the simultaneous increase of IL-6, TNF-α, and IL-10 in the current patients helps to substantiate the idea of a coordinated yet complex immune response to A. baumannii infection, with both inflammatory activation and immune counter-regulation. These cytokines have also been found to increase in Gram-negative bacterial sepsis and severe bacterial pneumonia [8, 22].

          In this study, IL-6 level was found to be significantly positively correlated with IL-10 level, while no significant correlation was found between IL-6 and TNF- α and between TNF-α and IL-10. The correlation between IL-6 and IL-10 was not very high and statistically insignificant, but it indicates that a negative effect of inflammation is accompanied by activation of anti-inflammatory processes. Biologically this interpretation is plausible, as IL-6 is a dominant pro-inflammatory mediator, while IL-10 is a mediator of immune regulation that prevents excess immune activation and tissue damage. Anti-inflammatory feedback responses, such as an increase in IL-10, have been reported to accompany inflammatory escalation, as in severe Gram-negative infections and sepsis [11, 22]. The current study also showed that, the higher serum levels of both IL-6 and TNF-α were significantly associated with the ICU admission, which most probably reflects the severity of infection and the systemic inflammatory burden in critically ill patients. The high concentrations of IL-6 and TNF-a in A. baumannii infection associated with ICU have been associated with macrophage activation, endothelial damage and clinical outcomes [8, 19]. In addition, the levels of IL-6, TNF-α and IL-10 were significantly elevated in patients with XDR isolates compared with patients with MDR isolates. This observation could suggest that there is a correlation between infections from these highly resistant strains and higher incidence of persistence of infection, later effective therapy, and higher immune dysregulation. Previous studies also showed that XDR A. baumannii infections are highly correlated with disease severity and poor prognosis especially in the ICU [18]. The parallel rise in IL-10 during XDR-associated infections also indicates the activation of compensatory anti-inflammatory mechanisms, which may be more of a response to greater inflammatory stimuli than a strictly protective one [7, 12].

5-Conclusion:

         Significant increase in the levels of IL-6, TNF- α and also IL-10 was observed in cases of Acinetobacter baumannii, suggesting strong inflammatory and immunoregulatory activation. These results indicate a significant correlation between the intensity of the immune reaction, severity of infection and antimicrobial resistance because of the higher cytokine levels observed in the cohort of ICU patients and the infections caused by XDR isolates. These results suggest that inflammatory cytokines could be used as markers to track severe A. baumannii infections and are valuable local data on the immunologic effects of highly resistant strains in Iraq.

Ethical approval and consent to participate

       It has been obtained. The study has been conducted after approval by the committee of Ethical issues, Kurdistan University of Medical Sciences (KUR-24) and the committee of Ethical issues of the University of Kufa (KUFA-51). Appropriate scientific and ethical committees provided ethical approval prior to the sampling and laboratory procedures. All those involved gave informed consent.

Competing interests:

The authors have no competing interests.

Funding

Nil

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About the authors

N. A. Hasan

Department of Microbiology, Faculty of Medicine, Kurdistan University of Medical Sciences, Iran;
Department of Criminal Evidence Sciences, Faculty of Medical Sciences, Jabir Ibn Hayyan University for Medical and Pharmaceutical Sciences, Iraq

Email: noor.a.hassan@jmu.edu.iq

M.Sc. Student  

Iraq

A. Taherpour

Department of Criminal Evidence Sciences, Faculty of Medical Sciences, Jabir Ibn Hayyan University for Medical and Pharmaceutical Sciences, Iraq

Email: are_taherpour@yahoo.com

Assistant professor, PhD

Iran, Islamic Republic of

A. A. Hussein

Department of Laboratory Investigations, Faculty of Science, University of Kufa, Iraq

Author for correspondence.
Email: ahmed.altwali@uokufa.edu.iq

Professor, PhD   

Iraq

References

Supplementary files