scholarly journals Characterization of Lymphocyte Response in the Female Genital Tract during Ascending Chlamydial Genital Infection in the Guinea Pig Model

2000 ◽  
Vol 68 (9) ◽  
pp. 5293-5298 ◽  
Author(s):  
Roger G. Rank ◽  
Anne K. Bowlin ◽  
Kathleen A. Kelly
Keyword(s):  
B Cells ◽  
Guinea Pig ◽  
Genital Tract ◽  
Primary Infection ◽  
Female Genital Tract ◽  
Challenge Infection ◽  
Pathologic Response ◽  
Genital Infection ◽  
Chemokine Production ◽  
Cd8 Cells

ABSTRACT It is well known that pathology caused by chlamydial infection is associated closely with the host response to the organism and that both innate and adaptive host responses contribute to tissue damage. While it is likely that the organism itself initiates the acute inflammatory response by eliciting cytokine and chemokine production from the host cell, the adaptive response is the result of activation of the cell-mediated immune response. While there are several studies describing the nature of the pathologic response in primate, guinea pig, and murine models, there is less information on the kinetics of the CD4 and CD8 response following primary and challenge infections. In this study, we have quantified by flow cytometry the mononuclear cell response to genital infection with the agent of guinea pig inclusion conjunctivitis in the cervix, endometrium, and oviducts at various times following a primary intravaginal infection and after a challenge infection. Tissues from individual animals were assessed for cells expressing CD4, CD8, or Mac-1 and for B cells. Peak responses of each subset occurred 10 to 14 days after a primary infection. The number of Mac-1-expressing cells in each tissue site was found to be dependent on the size of the inoculating dose of chlamydiae. The responses of each cell type were generally stronger in the cervix than in the upper genital tract. In contrast to the murine model but consistent with the primate models, there were equal numbers of CD4 and CD8 cells present in the infiltrates. Twenty-one days after challenge infection, which was performed 50 days after the primary infection, there was a significant increase in the number of CD4, CD8, and B cells in the oviduct compared to the number of these cells at the same time after a primary infection, providing clear cellular evidence for a cell-mediated immune pathologic response.

scholarly journals Local Host Response to Chlamydial Urethral Infection in Male Guinea Pigs

2010 ◽  
Vol 78 (4) ◽  
pp. 1670-1681 ◽  
Author(s):  
Yin Wang ◽  
Uma Nagarajan ◽  
Leah Hennings ◽  
Anne K. Bowlin ◽  
Roger G. Rank
Keyword(s):  
T Cells ◽  
Inflammatory Response ◽  
Primary Infection ◽  
Host Response ◽  
Challenge Infection ◽  
T Cell Response ◽  
Interleukin 12 ◽  
Genital Infection ◽  
Anamnestic Response ◽  
Necrosis Factor Alpha

ABSTRACT Very little is known about the host response to chlamydial genital infection in the male, particularly about the nature of the local response in the urethra. In this study, the pathological and immunologic responses to urethral infection of the male guinea pig with Chlamydia caviae (Chlamydophila caviae) were characterized both during a primary infection and following a challenge infection. A dose-response experiment found that the 50% infectious dose for male urethral infection was 78 inclusion-forming units. The histopathologic response was similar to that of the female, with an initial acute inflammatory response followed by a chronic inflammatory response and plasma cell infiltration. Production of IgG and IgA antibodies in local urethral secretions developed following infection, and levels of both increased in a typical anamnestic response following a challenge infection. CD4 and CD8 T cells, as well as B cells, were observed in the local site by flow cytometry, with a slightly increased number of CD8 cells. Following challenge infection, the dominant anamnestic response was solely in the B-cell compartment, with only a minimal number of T cells. The T-cell response was clearly a Th1 response, as judged by increased levels of gamma interferon (IFN-γ), interleukin-12 p40 (IL-12p40), and IL-2. The proinflammatory cytokines and chemokines IL-8, IL-1β, tumor necrosis factor alpha (TNF-α), CCL2 (monocyte chemoattractant protein 1 [MCP-1]), and CCL5 (RANTES) were elicited in the urethra following primary infection, but only CCL5 showed increased levels upon challenge. This study represents the first comprehensive analysis of the local immune response in the male urethra to a chlamydial genital infection.

scholarly journals Prior Genital Tract Infection with a Murine or Human Biovar of Chlamydia trachomatis Protects Mice against Heterotypic Challenge Infection

1999 ◽  
Vol 67 (6) ◽  
pp. 3019-3025 ◽  
Author(s):  
Kyle H. Ramsey ◽  
Todd W. Cotter ◽  
Rena D. Salyer ◽  
Gurwattan S. Miranpuri ◽  
Michael A. Yanez ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
Tract Infection ◽  
Genital Tract ◽  
Primary Infection ◽  
Secondary Infection ◽  
Delayed Type Hypersensitivity ◽  
Genital Infection ◽  
Blast Transformation ◽  
Genital Tract Infection ◽  
Igg Antibody

ABSTRACT We sought to assess the degree of cross-protective immunity in a mouse model of chlamydial genital tract infection. Following resolution of genital infection with the mouse pneumonitis (MoPn) biovar ofChlamydia trachomatis, mice were challenged intravaginally with either MoPn or human serovar E or L2. The majority of animals previously infected with MoPn were solidly immune to challenge with either of the two human biovars. Surprisingly, approximately 50% of animals became reinfected when homologously challenged with MoPn, although the secondary infection yielded significantly lower numbers of the organism isolated over a shorter duration than in the primary infection. Primary infection with serovar E also protected against challenge with MoPn or serovar L2, although the degree of immune protection was lower than that resulting from primary infection with MoPn. Blast transformation and assessment of delayed-type hypersensitivity indicated that mice previously infected with either human or murine biovars produced broadly cross-reactive T cells that recognized epitopes of either murine or human biovars of C. trachomatis. Immunoblotting demonstrated that primary MoPn infection produced immunoglobulin G (IgG) antibody to antigens of MoPn as well as at least three distinct antigenic components of human serovar E, one of which was identical in molecular weight to the major outer membrane protein (MOMP). Primary infection with serovar E produced IgG antibody reactive against serovar E but not MoPn MOMP and against at least one ca. 60-kDa protein of both chlamydial strains. Our results indicate that primary genital infection of mice with murineC. trachomatis induces immunity against challenge with either of two human biovars.

scholarly journals Immunity to Murine Chlamydia trachomatis Genital Tract Reinfection Involves B Cells and CD4+ T Cells but Not CD8+ T Cells

2000 ◽  
Vol 68 (12) ◽  
pp. 6979-6987 ◽  
Author(s):  
Sandra G. Morrison ◽  
Hua Su ◽  
Harlan D. Caldwell ◽  
Richard P. Morrison
Keyword(s):  
T Cells ◽  
B Cells ◽  
Chlamydia Trachomatis ◽  
B Cell ◽  
Genital Tract ◽  
Chlamydial Infection ◽  
Secondary Infection ◽  
Female Genital Tract ◽  
Immune Resistance ◽  
Deficient Mice

ABSTRACT CD4+ T-helper type 1 (Th1) responses are essential for the resolution of a primary Chlamydia trachomatis genital tract infection; however, elements of the immune response that function in resistance to reinfection are poorly understood. Defining the mechanisms of immune resistance to reinfection is important because the elements of protective adaptive immunity are distinguished by immunological memory and high-affinity antigen recognition, both of which are crucial to the development of efficacious vaccines. Using in vivo antibody depletion of CD4+ and CD8+ T cells prior to secondary intravaginal challenge, we identified lymphocyte populations that functioned in resistance to secondary chlamydial infection of the genital tract. Depletion of either CD4+ or CD8+ T cells in immune wild-type C57BL/6 mice had a limited effect on resistance to reinfection. However, depletion of CD4+ T cells, but not CD8+ T cells, in immune B-cell-deficient mice profoundly altered the course of secondary infection. CD4-depleted B-cell-deficient mice were unable to resolve a secondary infection, shed high levels of infectious chlamydiae, and did not resolve the infection until 3 to 4 weeks following the discontinuation of anti-CD4 treatment. These findings substantiated a predominant role for CD4+ T cells in host resistance to chlamydial reinfection of the female genital tract and demonstrated that CD8+ T cells are unnecessary for adaptive immune resistance. More importantly, however, this study establishes a previously unrecognized but very significant role for B cells in resistance to chlamydial reinfection and suggests that B cells and CD4+ T cells may function synergistically in providing immunity in this model of chlamydial infection. Whether CD4+ T cells and B cells function independently or dependently is unknown, but definition of those mechanisms is fundamental to understanding optimum protective immunity and to the development of highly efficacious immunotherapies against chlamydial urogenital infections.

scholarly journals Subclinical Chlamydial Infection of the Female Mouse Genital Tract Generates a Potent Protective Immune Response: Implications for Development of Live Attenuated Chlamydial Vaccine Strains

2000 ◽  
Vol 68 (1) ◽  
pp. 192-196 ◽  
Author(s):  
Hua Su ◽  
Ronald Messer ◽  
William Whitmire ◽  
Scott Hughes ◽  
Harlan D. Caldwell
Keyword(s):  
Immune Response ◽  
Genital Tract ◽  
Chlamydial Infection ◽  
Transmitted Disease ◽  
Female Genital Tract ◽  
Indirect Evidence ◽  
Protective Immune Response ◽  
Genital Infection ◽  
Cell Mediated Immunity ◽  
Female Genital

ABSTRACT Chlamydia trachomatis is a major cause of sexually transmitted disease (STD) for which a vaccine is needed. CD4+ T-helper type 1 (Th1) cell-mediated immunity is an important component of protective immunity against murine chlamydial genital infection. Conventional vaccine approaches have not proven effective in eliciting chlamydial-specific CD4 Th1 immunity at the genital mucosa. Thus, it is possible that the development of a highly efficacious vaccine against genital infection will depend on the generation of a live attenuated C. trachomatis vaccine. Attenuated strains of C. trachomatis do not exist, so their potential utility as vaccines cannot be tested in animal models of infection. We have developed a surrogate model to study the effect of chlamydial attenuation on infection and immunity of the female genital tract by treating mice with a subchlamydiacidal concentration of oxytetracycline following vaginal infection. Compared to untreated control mice, antibiotic-treated mice shed significantly fewer infectious organisms (3 log10) from the cervico-vagina, produced a minimal inflammatory response in urogenital tissue, and did not experience infection-related sequelae. Antibiotic-treated mice generated levels of chlamydia-specific antibody and cell-mediated immunity equivalent to those of control mice. Importantly, antibiotic-treated mice were found to be as immune as control untreated mice when rechallenged vaginally. These findings demonstrate that subclinical chlamydial infection of the murine female genital tract is sufficient to stimulate a potent protective immune response. They also present indirect evidence supporting the possible use of live attenuated chlamydial organisms in the development of vaccines against chlamydial STDs.

Role of the rodent acrosome and perforatorium in fertilization

1958 ◽  
Vol 149 (935) ◽  
pp. 241-248 ◽  
Keyword(s):  
Guinea Pig ◽  
Zona Pellucida ◽  
Golden Hamster ◽  
Genital Tract ◽  
Female Genital Tract ◽  
Chinese Hamster ◽  
Perivitelline Space ◽  
Cumulus Oophorus ◽  
Pass Through ◽  
Female Genital

A study has been made of the morphology of spermatozoa recovered from the female genital tract shortly after coitus, including spermatozoa entering and within eggs, in five rodent species. Elevation and loss of the acrosome was observed to occur in actively motile golden-hamster spermatozoa found in the cumulus oophorus and tubal fluid. Motile spermatozoa lacking the acrosome were also seen in the tubal fluid in guinea-pigs, in the cumulus oophorus in the guinea-pig and Libyan jird, and in the zona pellucida or perivitelline space of guinea-pig, golden-hamster, Chinese-hamster and jird eggs. It is concluded that the acrosome becomes modified in spermatozoa passing through the female genital tract and is detached before the spermatozoon penetrates the zona pellucida. These changes in the acrosome are considered to constitute ‘capacitation’. Removal of the acrosome exposes the perforatorium, which may carry a lysin capable of altering the zona substance in such a way as to permit the spermatozoon to pass through into the perivitelline space. The function of the acrosome is thought most likely to be the carriage of hyaluronidase, which probably enables the spermatozoon to pass through the cumulus oophorus. The separation of the nucleus from the perforatorium was observed in the vitellus of rat and golden-hamster eggs.

Ultrastructural Studies on Genital Infection with the Chlamydial Agent of Guinea Pig Inclusion Conjunctivitis

1977 ◽  
Vol 35 ◽  
pp. 352-353
Author(s):  
B. L. Soloff ◽  
A. L. Barron ◽  
H. J. White ◽  
R. G. Rank
Keyword(s):  
Guinea Pig ◽  
Sexual Contact ◽  
Chlamydia Psittaci ◽  
Genital Infection ◽  
Major Site ◽  
Ultrastructural Studies ◽  
Tissue Specimens ◽  
Guinea Pig Model ◽  
Adequate Tissue ◽  
Genital Tissue

Chlamydial organisms (specifically C. trachomatis) have been implicated as a frequent cause of genital infection in the human (1). Study of the histo- pathological aspects of such infections has been impeded because of difficulties in obtaining adequate tissue specimens and the lack of a suitable experimental host. In 1964, Murray (2) isolated the causative agent of guinea pig inclusion conjunctivitis which possesses similarities to human inclusion conjunctivitis. This guinea pig organism was found to be a member of the Chlamydia psittaci subgroup and was designated as the Gp-ic agent. Male guinea pigs have been successfully infected with Gp-ic by intraurethral inoculation. Transmission of the infection to the female by sexual contact has been demonstrated (3). We are not aware of any ultrastructural studies to date concerning the development of this agent in genital tissue.Studies in our laboratory have established that, in our guinea pig model, the cervix is the major site of injection.

EFFECT OF HIGH DOSES OF OESTROGEN AND PROGESTERONE ON THE NORADRENALINE CONTENT OF THE SHORT ADRENERGIC NEURONS INNERVATING THE MALE GENITAL TRACT OF THE RAT

1970 ◽  
Vol 64 (3) ◽  
pp. 459-465 ◽  
Author(s):  
Ch. Owman ◽  
N.-O. Sjöberg ◽  
N. O. Sjöstrand ◽  
G. Swedin
Keyword(s):  
Genital Tract ◽  
Reproductive Tract ◽  
Female Genital Tract ◽  
Total Content ◽  
Prolonged Treatment ◽  
Noradrenaline Content ◽  
Adrenergic Neurons ◽  
Short Adrenergic Neurons ◽  
High Doses ◽  
Male Genital

ABSTRACT The effect of prolonged treatment with high doses of oestrogen and/or progesterone on the amount of adrenergic transmitter in the short adrenergic neurons of the male reproductive tract of castrated rats has been studied by chemical determinations and histochemical demonstration of noradrenaline. Oestrogen, progesterone, or a combination of both, had no overt effect on the total content or on the concentration of noradrenaline in the male genital organs. The results are discussed in the light of recent findings that the content of the noradrenaline transmitter in the short adrenergic neurons to the female genital tract is markedly influenced by these female sex hormones.

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