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Previous studies have shown that males who have AIDS are more frequently affected by infectious diseases than females. The esophagus is the organ in the digestive tube that is more commonly affected by opportunistic infections during the syndrome. The aim of this study was to assess the influence of AIDS and of gender on local immunity of the esophageal epithelium. Fragments of the esophagus from 29 autopsied women and 37 autopsied men were collected at a university hospital from 1980 to 2009 and were divided in groups with and without AIDS. The IgA-, IgG-, and IgM-positive cells and Langerhans cells (LCs) were immunostained, respectively, with anti-IgA, anti-IgG, anti-IgM, and anti-S100. The software Image J was used to measure the esophageal epithelium and to count the epithelium cellular layers. Patients with AIDS, apart from gender, showed an increase in IgA-, IgG-, and IgM-positive cells and a reduction of Langerhans cells, in thickness and in number of cellular layers in the esophageal epithelium. However, among individuals with AIDS, men presented lower secretory expression of IgA-, IgG-, and IgM-positive cells than women and more intense reduction of LCs. Women have naturally presented better local esophageal immunity than men. Although AIDS possibly causes immunological and morphological alterations in the esophageal epithelium in both genders, women have better esophageal immunity, which may explain a greater frequency of hospital admissions due to infection of men with AIDS when compared with women.

We found that melatonin is the only hormone of the neuroendocrine system present in all systems, demonstrating synchronized biological rhythmic coordination and it is considered

Objective. To analyze the cytokines of the innate immune pulmonary response and the capacity for local response to melatonin according to the perinatal stress. Methods. 49 cases of pediatric autopsies were evaluated, divided according to cause of death, perinatal stress, gestational age, and birth weight. The percentages of IL-6, C-reactive protein (CRP), IL-1β, TNF-α, and melatonin receptor were evaluated by immunohistochemistry. Results. The IL-6 expression was higher in the children showing chronic stress, anoxia, and infection. The IL-6 expression showed a progressive increase according to the relation between weight and GA. There was no significant difference in the expression of IL-1β and TNF-α. The CRP expression was higher in the cases showing chronic stress and premature cases. The expression of melatonin receptors was significantly higher in the cases showing chronic stress, being more evident in the cases showing infection. Conclusion. The cause of death and the type of stress influence the expression in situ of melatonin and cytokines of the innate immune pulmonary response. The evaluation of IL-6 and CRP may contribute to the understanding of the evolution of neonates with chronic stress. The greater sensitivity of the lung to melatonin in these cases may indicate an attempt at controlling the immunological response, in an attempt to diminish the harmful effects of stress.

Anatomopathologic studies have failed to define the fetal inflammatory response syndrome (FIRS) as a cause of fetal death. Here, liver fragments of perinatal autopsies were collected at a university hospital from 1990 to 2009 and classified according to the cause of death, perinatal stress, and gestational age (GA) of the fetus. IL-6, TNF-α, and C-reactive protein (CRP) expression were immunostained, respectively, with primary antibody. Cases with congenital malformation, ascending infection, and perinatal anoxia showed increased IL-6, CRP, and TNF-α, respectively. Prematures presented higher expression of IL-6 whereas term births showed higher expression of CRP. Cases classified as acute stress presented higher expression of IL-6 and TNF-α and cases with chronic stress presented higher expression of CRP. GA correlated negatively with IL-6 and positively with CRP and TNF-α. Body weight correlated negatively with IL-6 and positively with CRP and TNF-α. Despite the diagnosis of FIRS being clinical and based on serum parameters, the findings in the current study allow the inference of FIRS diagnosis in the autopsied infants, based on an in situ liver analysis of these markers.

Acquired immunodeficiency syndrome (AIDS) is characterized by decreased immunity, making a patient more susceptible to opportunistic infections which can have cutaneous manifestations. The aim of this study was to evaluate the local immunity of the skin through morphological and immunohistochemical analysis. Skin samples of 52 women, 27 without AIDS and 25 with AIDS, autopsied in an academic referral hospital in Brazil were evaluated. The autopsy reports and medical records were reviewed, and histochemical Hematoxylin-eosin, Picrosirius red, and Verhoeff stains as well as morphometric (Image J and KS-300 Kontron-Zeiss) and immunohistochemical (S-100 and anti-IgA) analyses of the skin were performed. Women with AIDS presented a thinner epidermis than women without AIDS (33.33 [12.00-317.66] vs 67.42 [12.00-530.02] μm; p < 0.001), with a lower number of epithelial cell layers (4.00 [2.00-11.00] vs 4.00 [2.00-16.00]; p < 0.001), a smaller cell diameter (12.92 [6.00-28.87] vs 24.32 [6.00-33.12] μm; p < 0.001), and a lower number of Langerhans cells (LC) (12.58 [0.00-81.74] vs 31.44 [0.00-169.77] LC/mm(2); p < 0.001). The dermis contained more collagen fibers (8.20 % [2.40-19.40] vs 6.30 % [0.40-13.90]; p < 0.001). Some of these parameters were negatively correlated with viral load and positively correlated with the number of CD4+ T-lymphocytes. We conclude that a decrease of the local skin immunity in women with AIDS may contribute to the development of skin lesions.

Em pacientes com Síndrome da Imunodeficiência Adquirida há uma diminuição das células envolvidas na resposta imune, o que influencia na população celular dos folículos linfóides encontrados nas pregas vestibulares, favorecendo o aparecimento de infecções nas vias aéreas destes pacientes. Estas infecções são a principal causa de mortalidade e morbidade nestes pacientes. OBJETIVO: Caracterizar a população de células nos folículos linfóides localizados nas pregas vestibulares de adultos autopsiados com Síndrome da Imunodeficiência Adquirida, com e sem infecções respiratórias associadas. MATERIAIS E MÉTODOS: Foi realizado um estudo retrospectivo transversal em 64 laringes de adultos coletadas na rotina das autopsias. Para a imunohistoquímica foram utilizados os anticorpos: Anti-B cells, Anti-CD3, Anti-CD68 e Anti-follicular dendritic cells. RESULTADOS: 46 (71,87%) dos pacientes estudados tinham diagnóstico de Síndrome da Imunodeficiência Adquirida. Nestes pacientes, a celularidade dos folículos linfóides foi estatisticamente menor em relação ao grupo controle em todos os fenótipos estudados. Nos pacientes imunodeprimidos com infecção respiratória associada, o número de células estava diminuído, sendo significante no caso dos linfócitos T (p=0,024). CONCLUSÃO: Em nosso estudo demonstramos que os folículos linfóides das pregas vestibulares são afetados pela infecção viral e representam com fidedignidade o estado imunológico de imunodepressão destes pacientes.

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