title: Immune response to bacteria in seminiferous epithelium.
abstract: The luminal part of the seminiferous epithelium, a tissue compartment protected by the blood-testis barrier, has been considered a site of immune privilege. However, there are reports describing the production of anti-microbial peptides and the expression of Toll-like receptors in cells present in the seminiferous epithelium, evoking the possibility that this tissue compartment is immunologically active at least with regard to the innate immune response. To test this, we injected Escherichia coli into seminiferous tubules of live mice and examined the fate of bacteria, the production of chemokines and inflammatory cytokines, and the infiltration of neutrophils. The bacteria actively propagated and reached a maximal level in a day, but started to decrease after 5 days and completely disappeared in 2 months. The expression of macrophage inflammatory protein-2 and tumor necrosis factor-alpha became evident in macrophages present in the interstitial compartment of testes as early as 1-3 h after the inoculation of bacteria. Neutrophils first accumulated in the interstitial space at 9-12 h and entered the tubules after a day. On the other hand, impairment of spermatogenesis was observed a day after bacteria injection and seemed unrecoverable even after the bacteria were eliminated. By contrast, bacteria injected into the interstitial compartment were more rapidly cleared with no damage in the seminiferous epithelium. These results suggest the existence of immunity against invading microbes in the seminiferous epithelium although its effectiveness in maintaining tissue homeostasis remains equivocal.
authors.affiliation: Graduate School of Natural Science and Technology, Kanazawa University, Kanazawa, Ishikawa 920-1192, Japan.
authors.forename: Kaz
authors.initials: K
authors.lastname: Nagaosa
authors.forename: Chie
authors.initials: C
authors.lastname: Nakashima
authors.forename: Atsushi
authors.initials: A
authors.lastname: Kishimoto
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Nakanishi
mesh_terms: D000818:Animals; D058491:Bacterial Load; D054426:Chemokine CXCL2 / Q000235:genetics / Q000378:metabolism; D004926:Escherichia coli / Q000254:growth & development / Q000276:immunology*; D005786:Gene Expression Regulation; D018836:Inflammation Mediators / Q000378:metabolism; D008264:Macrophages / Q000276:immunology / Q000382:microbiology; D008297:Male; D051379:Mice; D020556:Neutrophil Infiltration; D009504:Neutrophils / Q000276:immunology / Q000382:microbiology; D012670:Seminiferous Epithelium / Q000276:immunology* / Q000382:microbiology*; D013091:Spermatogenesis; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D054426:Chemokine CXCL2; C404915:Cxcl2 protein, mouse; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha