Humoral immunity in the resolution of genital infection in female guinea pigs infected with the agent of guinea pig inclusion conjunctivitis

Rank, Roger G.; White, Harold J.; Barron, Almen L.

doi:10.1128/iai.26.2.573-579.1979

Cited by 100 publications

(61 citation statements)

References 16 publications

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“…However, in laboratory animals other than the mouse there has been controversy for a number of years over the relative role of antibody or cell mediated immunity in protection. Few of these experiments could be regarded as definitive from a modern perspective, but it appears that in the guinea pig specific antibodies may play a more prominent role in protection compared to the mouse [23,[26][27][28][29][30][31].…”

Section: Discussionmentioning

confidence: 99%

Studies in Knockout Mice Reveal that Anti‐Chlamydial Protection Requires TH1 Cells Producing IFN‐γ: Is this True for Humans?

et al. 1997

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Chlamydia trachomatis is one of the major causes of infertility and preventable blindness in the world. The organism is of particular interest from an immunological point of view because it is one of the few obligate intracellular bacterial pathogens. There is some evidence that repeated infections in humans stimulate protective immunity. However, until recently, it was unclear which components of the adaptive immune system give rise to protection. Studies in gene knockout mice reported here and elsewhere now give a coherent and cogent picture of the importance of the Th1 response, in particular IFN‐γ, for the localization and eradication of C. trachomatis genital tract infection. The key questions still to be addressed are the identity of the IFN‐γ responsive cells and whether the mouse is truly representative of host protection against chlamydiae in humans.

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Section: Discussionmentioning

confidence: 99%

Studies in Knockout Mice Reveal that Anti‐Chlamydial Protection Requires TH1 Cells Producing IFN‐γ: Is this True for Humans?

et al. 1997

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“…In this respect, previous studies have indicated that secretory immunoglobulin A (IgA) and IgG have protective roles during genital chlamydial infection (1-4, 21, 38). However, recent studies using experimental animal models of genital chlamydial disease have clearly established that T-cell-mediated immunity (CMI), usually involving gamma interferon (IFN-␥), is crucial for chlamydial control (5,8,13,14,16,18,29,30,33,34,36,37,41,44,45,49,52). Additional studies revealed that the resistance of experimental animals to genital reinfection by Chlamydia was associated with the pres-ence of relatively high intensity of antigen-specific T lymphocytes in the genital tract tissue (15).…”

Section: Genital Infection By the Obligate Intracellular Bacteriummentioning

confidence: 99%

Route of Infection That Induces a High Intensity of Gamma Interferon-Secreting T Cells in the Genital Tract Produces Optimal Protection against Chlamydia trachomatis Infection in Mice

et al. 1998

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The induction of local T helper type 1 (Th1)-mediated cellular immunity is crucial for resistance of mice to genital infection by the obligate intracellular bacterium Chlamydia trachomatis. We tested the hypothesis that the route of immunization that elicits relatively high numbers of chlamydia-specific, gamma interferon (IFN-␥)-secreting T lymphocytes (ISTLs) in the genital tract would induce optimal protective immunity against reinfection. Female BALB/c mice were infected intravaginally (i.v.), intranasally (i.n.), orally (p.o.), or subcutaneously (s.c.) with C. trachomatis. At days 7, 14, 21, and 28 postinfection, T cells isolated from the genital tract tissues were restimulated with chlamydial antigen in vitro, and the amounts of IFN-␥ induced were measured by a sandwiched enzyme-linked immunosorbent assay method. At day 7 postinfection, i.n.-and i.v.-immunized mice had high levels of chlamydia-specific ISTLs in their genital tracts (203.58 ؎ 68.1 and 225.5 ؎ 12.1 pg/ml, respectively). However, there were no detectable ISTLs in the genital tracts of p.o.-or s.c.-infected mice. When preinfected mice were challenged i.v. 70 days later, animals preexposed by the i.n. route were highly resistant to reinfection, with greatly reduced chlamydial burden, and suffered an attenuated infection that resolved by day 6 postchallenge. Animals preexposed by the i.v. route were modestly protected, whereas p.o. and s.c. groups were indistinguishable in this regard from control mice. The resistance of i.n.-immunized mice (and to some extent the i.v.-exposed mice) to reinfection was associated with early appearance (within 24 h) of high levels of genital ISTLs compared with mice preinfected by other routes. Furthermore, although i.n. and i.v.-immunized mice had comparable levels of chlamydia-specific immunoglobulin A (IgA) antibodies in their vaginal washes, the levels of IgG2a were four-sixfold higher in i.n.-immunized mice than in any of the other groups. The results suggested that immunization routes that foster rapid induction of vigorous genital mucosal cell-mediated immune (CMI) effectors (e.g., IFN-␥), the CMI-associated humoral effector, IgG2a, and to some extent secretory IgA produce protective immunity against chlamydial genital infection. Therefore, i.n. immunization is a potential delivery route of choice in the development of a vaccine against Chlamydia.

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“…In the female genital tract, the shedding of the infected cells from the cervical epithelium results in their migration down the genital tract to the vagina. This was actually observed over and over when we collected secretions and cells from the vagina and quantified the percentage of cells infected with GPIC ( Barron et al, 1979;Rank et al, 1979). We routinely observed apparently healthy cells with inclusions at all stages of the developmental cycle as well as large numbers of PMNs.…”

Section: Discussionmentioning

confidence: 80%

Chlamydiae and polymorphonuclear leukocytes: unlikely allies in the spread of chlamydial infection

Rank

Whittimore

Bowlin

et al. 2008

FEMS Immunology &Amp; Medical Microbiology

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While much is known about the attachment of the chlamydiae to the host cell and intracellular events during the developmental cycle, little is known about the mechanism(s) by which elementary bodies exit the cell. In this report, we use the guinea pig conjunctival model of Chlamydia caviae infection to present in vivo ultrastructural evidence supporting two mechanisms for release of chlamydiae from the mucosal epithelia. Four days after infection, histopathologic observation shows an intense infiltration of polymorphonuclear leukocytes (PMN) in the conjunctival epithelium. By transmission electron microscopy, a gradient-directed PMN response to chlamydiae-infected epithelial cells was observed. As PMN infiltration intensifies, epithelial hemidesmosome/integrin/focal adhesion adherence with the basal lamina is disconnected and PMNs literally lift off and release infected superficial epithelia from the mucosa. Many of these infected cells appear to be healthy with intact microvilli, nuclei, and mitochondria. While lysis of some infected cells occurs with release of chlamydiae into the extracellular surface milieu, the majority of infected cells are pushed off the epithelium. We propose that PMNs play an active role in detaching infected cells from the epithelium and that these infected cells eventually die releasing organisms but, in the process move to new tissue sites via fluid dynamics.

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Humoral immunity in the resolution of genital infection in female guinea pigs infected with the agent of guinea pig inclusion conjunctivitis

Cited by 100 publications

References 16 publications

Studies in Knockout Mice Reveal that Anti‐Chlamydial Protection Requires TH1 Cells Producing IFN‐γ: Is this True for Humans?

Studies in Knockout Mice Reveal that Anti‐Chlamydial Protection Requires TH1 Cells Producing IFN‐γ: Is this True for Humans?

Route of Infection That Induces a High Intensity of Gamma Interferon-Secreting T Cells in the Genital Tract Produces Optimal Protection against Chlamydia trachomatis Infection in Mice

Chlamydiae and polymorphonuclear leukocytes: unlikely allies in the spread of chlamydial infection

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