Distinct Intensity of Host-Pathogen Interactions in Chlamydia psittaci- and Chlamydia abortus-Infected Chicken Embryos

Braukmann, Maria; Sachse, Konrad; Jacobsen, Ilse D.; Westermann, Martin; Menge, Christian; Saluz, Hans‐Peter; Berndt, Angela

doi:10.1128/iai.00437-12

Cited by 28 publications

(20 citation statements)

References 55 publications

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“…Chlamydia ( pneumoniae ) has been demonstrated to use alveolar macrophages and peripheral blood monocytes as ‘Trojan horses’ for covert dissemination [43]. Indeed, as we and others [44] have shown for spleen tissue, C. psittaci DC 15 disseminates after lung infection in the host. For this reason, opsonization could be assisting the intracellular bacterium early in infection.…”

Section: Discussionmentioning

confidence: 81%

A New Role of the Complement System: C3 Provides Protection in a Mouse Model of Lung Infection with Intracellular Chlamydia psittaci

et al. 2012

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The complement system modulates the intensity of innate and specific immunity. While it protects against infections by extracellular bacteria its role in infection with obligate intracellular bacteria, such as the avian and human pathogen Chlamydia (C.) psittaci, is still unknown. In the present study, knockout mice lacking C3 and thus all main complement effector functions were intranasally infected with C. psittaci strain DC15. Clinical parameters, lung histology, and cytokine levels were determined. A subset of infections was additionally performed with mice lacking C5 or C5a receptors. Complement activation occurred before symptoms of pneumonia appeared. Mice lacking C3 were ∼100 times more susceptible to the intracellular bacteria compared to wild-type mice, with all C3−/− mice succumbing to infection after day 9. At a low infective dose, C3−/− mice became severely ill after an even longer delay, the kinetics suggesting a so far unknown link of complement to the adaptive, protective immune response against chlamydiae. The lethal phenotype of C3−/− mice is not based on differences in the anti-chlamydial IgG response (which is slightly delayed) as demonstrated by serum transfer experiments. In addition, during the first week of infection, the absence of C3 was associated with partial protection characterized by reduced weight loss, better clinical score and lower bacterial burden, which might be explained by a different mechanism. Lack of complement functions downstream of C5 had little effect. This study demonstrates for the first time a strong and complex influence of complement effector functions, downstream of C3 and upstream of C5, on the outcome of an infection with intracellular bacteria, such as C. psittaci.

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Section: Discussionmentioning

confidence: 81%

A New Role of the Complement System: C3 Provides Protection in a Mouse Model of Lung Infection with Intracellular Chlamydia psittaci

et al. 2012

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“…C. psittaci infections of chicken embryos also caused a drastically higher mortality rate than was observed for the infections with C. abortus . It also beat C. abortus by spreading more extensively within the organs of infected hosts, increasing the amount of proinflammatory mediators as well as the number of macrophages . Furthermore, C. psittaci seems to subvert host immunity and thereby modulate its virulence .…”

Section: Chlamydia Psittaci–host Cell Interaction—attachment Intracementioning

confidence: 99%

“…To what extent, and via which mechanisms, C. psittaci is able to subvert the immune response of infected hosts is not understood. However, there are strong indications that C. psittaci is able to cope with proinflammatory effectors in infected chickens (embryos or young animals) much more successfully than other chlamydiae. Moreover, upregulation of ftsW (replication), incA (inclusion stabilization), CPAF (protein processing ), and groEL (molecular chaperone) seem to mirror specific C. psittaci properties needed for the successful establishment and further dissemination of the infection in the host .…”

Section: Cell‐autonomous Innate and Adaptive Immune Responses Againmentioning

confidence: 99%

Chlamydia–host cell interaction not only from a bird's eye view: some lessons from Chlamydia psittaci

et al. 2016

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Edited by Wilhelm JustChlamydia psittaci causes psittacosis/ornithosis in birds and is an economically important pathogen for poultry farming. It also infects nonavian domestic animals as well as rodents, and is a zoonotic human pathogen responsible for atypical pneumonia. The bacterium efficiently disseminates in host organisms causing pulmonary and systemic disease. Its rapid entry, fast replication cycle, and tight control of intracellular transport routes contribute to the host-to-host transmission and efficient growth observed with C. psittaci. Recent studies have revealed that the pathogen copes better than other chlamydial strains with proinflammatory effectors produced during the early immune reaction of infected hosts. These features likely contribute to successful infections and might explain the potent adaptation and evasion characteristics of the agent. Current findings on cell-autonomous, innate, and adaptive defenses against C. psittaci provide novel insights into the concerted immune mechanisms involved in the clearance of the pathogen. Further in-depth studies on C. psittaci and other related agents in cellular as well as animal models are needed to develop more efficient antichlamydial therapies and vaccination strategies.

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“…psittaci seems to be particularly efficient in escaping from the innate immune response of the host. This conclusion was drawn from the data of an experimental study by Braukmann and colleagues [74] comparing C. psittaci and C. abortus infection in embryonated chicken eggs (see also the "Lessons Learned from Animal Models" section). When confronted with the release of pro-inflammatory mediators during early host response, the pathogen was shown to react with up-regulation of essential genes [74].…”

Section: New Insights Into Host Immune Response To Chlamydial Infectionmentioning

confidence: 99%

“…This conclusion was drawn from the data of an experimental study by Braukmann and colleagues [74] comparing C. psittaci and C. abortus infection in embryonated chicken eggs (see also the "Lessons Learned from Animal Models" section). When confronted with the release of pro-inflammatory mediators during early host response, the pathogen was shown to react with up-regulation of essential genes [74]. This included elevated mRNA expression rates of chlamydial IncA (involved in stabilisation of the inclusion), ftsW (regulating binary fission of RBs), groEL (chaperone associating with macrophages) and cpaf (involved in processing of host proteins controlling the integrity of the inclusion).…”

Section: New Insights Into Host Immune Response To Chlamydial Infectionmentioning

confidence: 99%

Avian Chlamydiosis

Sachse

Laroucau

Vanrompay

2015

Curr Clin Micro Rpt

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Recent findings in research on avian chlamydiosis include an increase in the reported prevalence of Chlamydia (C.) psittaci in poultry flocks, detailed descriptions of molecular processes governing the course of infection in vivo, as well as the discovery of new chlamydial species. Here we review the major advances of the last 6 years. In particular, we suggest that the observed re-emergence of C. psittaci infections in domestic poultry are due to a reduction in the use of antibiotics and better diagnostic assays. Cellular and animal models have significantly contributed to improving our understanding of the pathogenesis, including the events leading to systemic disease. The elucidation of host-pathogen interactions revealed the efficiency of C. psittaci in proliferating and disseminating despite the action of pro-inflammatory mediators and other factors during host immune response. Finally, the recent introduction of C. avium and C. gallinacea sheds new light on the epidemiology and aetiopathology of avian chlamydiosis.

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Distinct Intensity of Host-Pathogen Interactions in Chlamydia psittaci- and Chlamydia abortus-Infected Chicken Embryos

Abstract: ABSTRACTFactors and mechanisms determining the differences in virulence and host specificity between the zoonotic agentsChlamydia psittaciandChlamydia abortusare still largely unknown. In the present study, two strai… Show more

Cited by 28 publications

References 55 publications

A New Role of the Complement System: C3 Provides Protection in a Mouse Model of Lung Infection with Intracellular Chlamydia psittaci

A New Role of the Complement System: C3 Provides Protection in a Mouse Model of Lung Infection with Intracellular Chlamydia psittaci

Chlamydia–host cell interaction not only from a bird's eye view: some lessons from Chlamydia psittaci

Avian Chlamydiosis

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