Immuno‐competent cells in the murine epididymis following infection with Escherichiu coli

Abstract

Epididymitis was induced by retrograde injection of Escherichia coli into the vas deferens of 28 mice. A group of 28 saline-injected animals served as controls. On Days 1, 3, 7 and 28, groups of seven animals were killed. Bacterial culture was performed. Leucocyte numbers and distribution were determined in epididymides. In infected mice, E. coli were isolated from all epididymides on Days 1 and 3, but only from five of seven epididymides on Days 7 and 28. One week after infection, the total number of macrophages rose from about 10 to 28%. Significantly increased macrophage percentages were also found in animals killed 28 days after infection. A simultaneous increase in MHC class II positive cells was seen on Day 7. A total of 20% of the cells expressed MHC class II in infected epididymides (normal = 6%). A similar increase was found on Day 28 after infection. Most of the macrophages and MHC class II positive cells were located in the interstitium, fewer in the peritubular layer and nearly none in the epithelium. The main increase in these cells occurred in the interstitium and, to a lesser but significant extent, in the peritubular area. T-helper and T-suppressor/cytotoxic lymphocytes reached peak values on Day 28. The increase in T-lymphocytes and simultaneous appearance of plasma cells followed the increase in numbers of macrophages and MHC class II positive cells. They were located mainly in the interstitium. A sequential increase in leucocyte subsets and negative culture results for E. coli were observed on Days 7 and 28 (2/7 on each day). The inflammatory process was restricted to the interstitium.(ABSTRACT TRUNCATED AT 250 WORDS)

Experimental Escherichia coli epididymitis in rats: a model to assess the outcome of antibiotic treatment

“…The immune system eradicated the pathogen in several epididymes 3 and 6 months after infection. That immune mechanisms may clear the epididymal aspirate and tissue from pathogens in a proportion of cases has been reported previously in the rabbit [9] and mouse [11] models of experimental E. coli epididymitis. Nashan et al [11] suggested that successful phagocytotic activity of macrophages was the predominant mechanism, by characterizing the sequence of cellular events using monoclonal antibodies.…”

“…That immune mechanisms may clear the epididymal aspirate and tissue from pathogens in a proportion of cases has been reported previously in the rabbit [9] and mouse [11] models of experimental E. coli epididymitis. Nashan et al [11] suggested that successful phagocytotic activity of macrophages was the predominant mechanism, by characterizing the sequence of cellular events using monoclonal antibodies. However, in contrast to other reports [9,14], although E. coli was not detected in the present contralateral epididymis, with no antimicrobial treatment viable pathogens could be re-isolated up to 3 months after the initial infection in epididymal and up to 6 months later in prostate tissue.…”

“…In a model of acute epididymitis, locally produced interleukins, particularly interleukin-6, have been suggested to be important in early priming of the immune response in experimental bacterial epididymitis, and in reducing the extension of local bacterial infection [23]. In a murine model of E. coli epididymitis, there were more T helper and T suppressor/ cytotoxic cells 4 weeks after infection, in addition to more macrophages and MHC class II expression in the absence of the pathogen [11]. It was concluded by the sequence of cellular responses that an immunologically active process may lack apparent down-regulation.…”

“…However, against which epitope the immunological answer is directed is unknown. As this pattern of cellular response renders antisperm antibody formation possible [11], and as circulating antisperm antibodies in serum against sperm have been found in a rat model of E. coli epididymitis [13], some kind of autoimmune mechanism has been proposed. Second, after phagocytosis, macrophages may present E. coli fragments as antigen and thereby stimulate a cascade for a persistent immune response.…”

“…However, instead of adequate antimicrobial treatment, the development of chronic inflammation with its implications for impaired male fertility is unpredictable [4]. Animal models are necessary to analyse the pathological mechanisms of epididymal and testicular damage [9][10][11][12], and the effect of antimicrobial agents on the grade of inflammation [13][14][15].…”