scholarly journals Immunopathogenesis of recurrent vulvovaginal candidiasis.

1996 ◽  
Vol 9 (3) ◽  
pp. 335-348 ◽  
Author(s):  
P L Fidel ◽  
J D Sobel
Keyword(s):  
Host Defense ◽  
Defense Mechanism ◽  
Peripheral Circulation ◽  
Vulvovaginal Candidiasis ◽  
Cell Mediated Immunity ◽  
Vaginal Mucosa ◽  
Childbearing Age ◽  
Vaginal Infections ◽  
Recurrent Vulvovaginal Candidiasis ◽  
Host Defense Mechanism

Recurrent vulvovaginal candidiasis (RVVC) is a prevalent opportunistic mucosal infection, caused predominantly by Candida albicans, which affects a significant number of otherwise healthy women of childbearing age. Since there are no known exogenous predisposing factors to explain the incidence of symptomatic vaginitis in most women with idiopathic RVVC, it has been postulated that these particular women suffer from an immunological abnormality that prediposes them to RVVC. Because of the increased incidence of mucosal candidiasis in individuals with depressed cell-mediated immunity (CMI), defects in CMI are viewed as a possible explanation for RVVC. In this review, we attempt to place into perspective the accumulated information regarding the immunopathogenesis of RVVC, as well as to provide new immunological perspectives and hypotheses regarding potential immunological deficiencies that may predispose to RVVC and potentially other mucosal infections by the same organism. The results of both clinical studies and studies in an animal model of experimental vaginitis suggest that systemic CMI may not be the predominant host defense mechanism against C. albicans vaginal infections. Rather, locally acquired mucosal immunity, distinct from that in the peripheral circulation, is now under consideration as an important host defense at the vaginal mucosa, as well as the notion that changes in local CMI mechanism(s) may predispose to RVVC.

scholarly journals Local Production of Chemokines during Experimental Vaginal Candidiasis

1999 ◽  
Vol 67 (11) ◽  
pp. 5820-5826 ◽  
Author(s):  
Michael Saavedra ◽  
Brad Taylor ◽  
Nicholas Lukacs ◽  
Paul L. Fidel
Keyword(s):  
T Cells ◽  
Host Defense ◽  
Defense Mechanism ◽  
Polymorphonuclear Neutrophils ◽  
Vaginal Candidiasis ◽  
Cell Mediated Immunity ◽  
Vaginal Mucosa ◽  
Childbearing Age ◽  
Vaginal Tissue ◽  
Fungal Burden

ABSTRACT Recurrent vulvovaginal candidiasis, caused by Candida albicans, is a significant problem in women of childbearing age. Although cell-mediated immunity (CMI) due to T cells and cytokines is the predominant host defense mechanism againstC. albicans at mucosal tissue sites, host defense mechanisms against C. albicans at the vaginal mucosa are poorly understood. Based on an estrogen-dependent murine model of vaginal candidiasis, our data suggest that systemic CMI is ineffective against C. albicans vaginal infections. Thus, we have postulated that local immune mechanisms are critical for protection against infection. In the present study, the kinetic production of chemokines normally associated with the chemotaxis of T cells, macrophages (RANTES, MIP-1α, MCP-1), and polymorphonuclear neutrophils (MIP-2) was examined following intravaginal inoculation ofC. albicans in estrogen-treated or untreated mice. Results showed significant increases in MCP-1 protein and mRNA in vaginal tissue of infected mice as early as 2 and 4 days postinoculation, respectively, that continued through a 21-day observation period, irrespective of estrogen status. No significant changes were observed with RANTES, MIP-1α, or MIP-2, although relatively high constitutive levels of RANTES mRNA and MIP-2 protein were observed. Furthermore, intravaginal immunoneutralization of MCP-1 with anti-MCP-1 antibodies resulted in a significant increase in vaginal fungal burden early during infection, suggesting that MCP-1 plays some role in reducing the fungal burden during vaginal infection. However, the lack of changes in leukocyte profiles in vaginal lavage fluids collected from infected versus uninfected mice suggests that MCP-1 functions to control vaginal C. albicans titers in a manner independent of cellular chemotactic activity.

scholarly journals Chlamydia trachomatis Infection Does Not Enhance Local Cellular Immunity against Concurrent CandidaVaginal Infection

2001 ◽  
Vol 69 (5) ◽  
pp. 3451-3454 ◽  
Author(s):  
Kathleen A. Kelly ◽  
Heather L. Gray ◽  
Jennifer C. Walker ◽  
Roger G. Rank ◽  
Floyd L. Wormley ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
Genital Tract ◽  
Defense Mechanism ◽  
Host Responses ◽  
Cell Mediated Immunity ◽  
Vaginal Mucosa ◽  
Genital Tract Infection ◽  
Chlamydia Trachomatis Infection ◽  
Host Defense Mechanism ◽  
Tract Infections

ABSTRACT Although Th1-type cell-mediated immunity (CMI) is the predominant host defense mechanism against mucosal Candida albicansinfection, CMI against a vaginal C. albicans infection in mice is limited at the vaginal mucosa despite a strongCandida-specific Th1-type response in the draining lymph nodes. In contrast, Th1-type CMI is highly effective against an experimental Chlamydia trachomatis genital tract infection. This study demonstrated through two independent designs that a concurrent Candida and Chlamydia infection could not accelerate or modulate the anti-Candida CMI response. Together, these results suggest that host responses to these genital tract infections are independent and not influenced by the presence of the other.

scholarly journals Human Serum Albumin Is an Essential Component of the Host Defense Mechanism Against Clostridium difficile Intoxication

2018 ◽  
Vol 218 (9) ◽  
pp. 1424-1435 ◽  
Author(s):  
Alessandra di Masi ◽  
Loris Leboffe ◽  
Fabio Polticelli ◽  
Federica Tonon ◽  
Cristina Zennaro ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Human Serum Albumin ◽  
Serum Albumin ◽  
Human Serum ◽  
Host Defense ◽  
Defense Mechanism ◽  
Essential Component ◽  
Host Defense Mechanism

scholarly journals Autophagy-activating strategies to promote innate defense against mycobacteria

2019 ◽  
Vol 51 (12) ◽  
pp. 1-10 ◽  
Author(s):  
Yi Sak Kim ◽  
Prashanta Silwal ◽  
Soo Yeon Kim ◽  
Tamotsu Yoshimori ◽  
Eun-Kyeong Jo
Keyword(s):  
Host Defense ◽  
Defense Mechanism ◽  
Multidrug Resistant ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Innate Defense ◽  
Host Defense Mechanism ◽  
A Cell

AbstractMycobacterium tuberculosis (Mtb) is a major causal pathogen of human tuberculosis (TB), which is a serious health burden worldwide. The demand for the development of an innovative therapeutic strategy to treat TB is high due to drug-resistant forms of TB. Autophagy is a cell-autonomous host defense mechanism by which intracytoplasmic cargos can be delivered and then destroyed in lysosomes. Previous studies have reported that autophagy-activating agents and small molecules may be beneficial in restricting intracellular Mtb infection, even with multidrug-resistant Mtb strains. Recent studies have revealed the essential roles of host nuclear receptors (NRs) in the activation of the host defense through antibacterial autophagy against Mtb infection. In particular, we discuss the function of estrogen-related receptor (ERR) α and peroxisome proliferator-activated receptor (PPAR) α in autophagy regulation to improve host defenses against Mtb infection. Despite promising findings relating to the antitubercular effects of various agents, our understanding of the molecular mechanism by which autophagy-activating agents suppress intracellular Mtb in vitro and in vivo is lacking. An improved understanding of the antibacterial autophagic mechanisms in the innate host defense will eventually lead to the development of new therapeutic strategies for human TB.

Pathogenesis of thrombosis

Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 255-258 ◽  
Author(s):  
Bruce Furie
Keyword(s):  
High Pressure ◽  
Host Defense ◽  
Intravital Microscopy ◽  
Defense Mechanism ◽  
Tissue Injury ◽  
Thrombus Formation ◽  
Animal Experiments ◽  
Circulatory System ◽  
Live Animal ◽  
Host Defense Mechanism

Abstract The hemostatic process is a host defense mechanism to preserve the integrity of the closed high pressure circulatory system. This process must remain inactive but poised to minimize extravasation of blood from the vasculature following tissue injury. Given the complexity of the hemostatic mechanism, paradigms developed from biochemical and cell biological approaches have been revisited by studying thrombus formation in a live animal by intravital microscopy. Many of these paradigms have proven accurate, but others need to be reconsidered given the results of whole animal experiments.

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