Vol 23, No 1 (2020)

Acne (Ac) represents a widespread dermatosis most commonly found in adolescents and adults covering 6-85% total cases. It has been traditionally believed that Propionibacterium acnes (P. acnes) colonizes ducts of the sebaceous hair follicles (SHFs), activates innate immune response and triggers transition of non-inflammatory erosions (comedones) into inflammatory lesions such as papules, pustules and nodules. Moreover, it was also shown that inflammatory reaction develops at late Ac stage and its severe course. Today, it has been evidenced that Ac-coupled inflammation develops at all stages of dermatosis, perhaps in a subclinical manner, even prior to emergence of comedones.

It is commonly accepted that acne targets SHFs displaying location-related marked morphological, microbiological and metabolic diversity. For instance, SHFs is profoundly affected by altered hormone and immunological properties as well as environmental cues.

Comparative studies examining efficacy nd medicated therapy with anti-inflammatgory potential evidence about early inflammatory reaction related to acne.

The data obtained confirm that P. acnes elicits inflammatory reaction in acne that additionally maintains P. acnes proliferation. It was found that P. acnes initiates TLR2-mediated innate immune reaction both at early and late stages of developing dermatosis. Such reaction results in upregulated immune genes including those encoding cytokines and chemokines recruiting immune cells.

Today, owing to clinical, immunological, histology and immunohistochemistry data there has been accumulated evidence confirming significance of ongoing inflammation as a pathophysiological basis for emerging acne.

Upon that, pathophysiological mechanisms triggering inflammatory reaction in acne are complex and poorly investigated, thereby underlying a need to conduct further studies.

Research objective – to reveal gender-related features of changes in immune status during acute ischemic stroke.

There were enrolled 160 subjects including 100 (50 males and 50 females) apparently healthy (no complaints, no check-ups and no diagnoses). On admission, 60 (30 males and 30 females) were diagnosed with ischemic stroke, who were examined for changes in immune status by assessing the following parameters such as T and B-cell subsets: peripheral blood CD3+ (mature T lymphocytes); CD4+ (T helper); CD8+ (cytotoxic T cells) T cells; CD16+ (natural killers); CD20+ (B cells) cells as well as CD4/CD8 ratio. Total amount of IgG, M, A antibodies was measured by simple radial immunodiffusion by Mancini et al., whereas IgE level – by ELISA. Level of serum C3-, C4-complement components, TNFα, IL-1β, IL-2, IL-6, IL-8, INFγ, IL-4, IL-10 was measured by ELISA.

Our study revealed that in peripheral blood count of total leukocytes, band neutrophils and lymphocytes was significantly increased in acute ischemic stroke vs healthy subjects in sex-independent manner. Moreover, no pronounced differences between females vs males were observed. Rise in such parameters may be due to host inflammatory response. While examining humoral immunity, it was shown that activity the complement system and cytokine level in patients with acute ischemic stroke had gender-related increase in pro-inflammatory cytokines IL-1β, IL-6, IL-8, IL-2 that paralleled with decreased anti-inflammatory IL-10, IL-4 and IFNγ. In addition, subjects in both groups demonstrated significantly increased amount of IgG, IgM, IgE, total complement and its С3- and C4 fractions, C1-inhibitor, CIC, factor H, FI, FH, NBT-sp., NBI-st. hence, based on this it may be concluded that patients with ischemic stroke exert signs of marked inflammation. Similar to cellular immune arm, the above parameters revealed gender-related differences so that all immune parameters were significantly increased in males vs females.

Previous studies found some associations between immunoglobulin class A antibodies specific to benzo[a]pyrene (IgA-Bp), estradiol (IgA-Es) and progesterone (IgA-Pg) as well as breast cancer (BC) in females and lung cancer (LC) in males. It was suggested that such antibodies affect serum Es and Pg levels.

Our study was aimed at revealing putative features of mutual effects of IgA-Bp, IgA-Es and IgA-Pg on serum Es and Pg level both in healthy and BC females as well as healthy and LC males.

Serum levels of Es and Pg and IgA-Bp, IgA-Es and IgA-Pg were measured by ELISA in 190 nonsmoking healthy and 518 BC females as well as 312 smoking healthy and 196 LC males.

It was found that healthy subjects vs cancer patients prominently differed by assessing individual Pg/Es ratios: healthy vs BC females had it set at 6.6 vs 2.9 (p < 0.0001), respectively, whereas in healthy vs LC males it was at 5.2 vs 10.1 (p < 0.0001), respectively.

Individual Pg/Es ratio paralleled in healthy females with high vs low IgA-Bp/IgA-Pg > 1.5 and IgA-Es/IgA-Pg > 1.5 ratios (3.5 vs 9.7, p < 0.0001). No T such associations were observed in BC patients. In addition, the lowest individual Pg/Es ratio in healthy males was found together with IgA-Es/ IgA-Pg > 1.5 ratios accompanied with IgA-Bp/IgA-Pg ≤ 1.5 (2.9) and peaked in case of concurrently low IgA-Bp/IgA-Pg ≤ 1.5 and IgA-Es/IgA-Pg ≤ 1.5 (5.2, p = 0.005) or high IgA-Bp/IgA-Pg > 1.5 and IgA-Es/IgA-Pg > 1.5 (6.5, p = 0.002). In contrast, the lowest Pg/Es ratio (7.4) was revealed in LC patients simultaneously bearing high IgA-Bp/IgA-Pg > 1.5 and low IgA-Es/IgA-Pg ≤ 1.5 ratios compared to simultaneously low ratios (11.3, p = 0.002).

In conclusion, individual Pg/Es ratios depended on individual IgA-Bp/IgA-Pg and IgA-Es/IgA-Pg ratios. A cooperative influence of serum antibodies specific to environmental chemical carcinogens and endogenous steroids on hormone balance was featured both in healthy subjects as well as BC females and LC males.

The data obtained may be useful while developing new strategies to cancer prevention: by using selective modulators of estrogen receptors and aromatase inhibitors as well as for development of anticancer vaccines.