T Cell Chemotaxis and Chemokine Release after<i>Staphylococcus aureus</i>Interaction with Polarized Airway Epithelium

Escotte, Sandie; Alam, Denise Al; Naour, Richard Le; Puchelle, Édith; Guenounou, Moncef; Gangloff, Sophie C.

doi:10.1165/rcmb.2005-0191oc

Cited by 30 publications

(29 citation statements)

References 36 publications

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“…The role of CXC chemokines in the pulmonary pathology associated with S. aureus infection has been previously described (2,7). These investigators demonstrated that S. aureus alpha-toxin, which is expressed by the USA300 strain used in our studies, induces the expression of the CXC chemokines and the associated pathology (2).…”

Section: Discussionsupporting

confidence: 67%

Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

et al. 2011

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Staphylococcus aureus causes especially severe pulmonary infection, associated with high morbidity and mortality. In addition to the effects of specific virulence factors, it appears that the intensity of the host proinflammatory response, particularly in the initial stages of infection, contributes substantially to pulmonary damage. We tested the hypothesis that the CD11c ؉ leukocytes are important in the host response to pulmonary infection with methicillin-resistant S. aureus (MRSA) USA300. Clodronate-induced depletion of the alveolar macrophage population resulted in increased numbers of dendritic cells (DCs) and CD4؉ cells in bronchoalveolar lavage (BAL) fluid and was associated with significantly increased mortality by 18 h following S. aureus inoculation but had no effect on bacterial load or polymorphonuclear leukocyte (PMN) numbers in the lung. These clodronate-treated mice also had increased expression of interleukin-17A/F (IL-17A/F) and Staphylococcus aureus bacteria, particularly the epidemic methicillin-resistant USA300 strains, have recently been associated with severe invasive pneumonias in previously well individuals, as well as being a complication of influenza (15). These pneumonias are characterized by a predominant polymorphonuclear leukocyte (PMN) response with significant areas of necrosis and hemorrhage (6). Numerous studies have addressed which of the several virulence factors expressed by the USA300 strains are most important in the pathogenesis of pulmonary infection. In the C57BL/6J mouse model of acute pneumonia, the contributions of ␣-hemolysin (Hla) (3) and protein A (SpA) (8) have been well documented. The importance of Panton-Valentine leukocidin (PVL) has also been confirmed in a rabbit model of infection; rabbits, like humans, have highly PVL-susceptible leukocytes (6). Besides the direct toxicity of staphylococcal toxins, some of the pathological consequences of staphylococcal virulence factors are due to the intensity of the host immune response. Both Tnfr1 Ϫ/Ϫ (8) and Ifnar Ϫ/Ϫ (17) mice are highly resistant to S. aureus pneumonia and even to the USA300 strains expressing these virulence factors, suggesting that the intensity of the host immune response to infection is critical in the pathogenesis of severe pneumonia.Exactly which components of the innate immune response contribute to lethality in these models of acute S. aureus pneumonia has not been clearly delineated. PMNs have long been thought to be critical for efficient staphylococcal clearance (19,22), and the increased incidence of severe staphylococcal infection in humans with disorders of PMN function or activation, such as chronic granulomatous disease (10, 12), confirm this observation. PMNs themselves can also contribute to the pathology associated with staphylococcal infection. A substantial component of the lung pathology associated with S. aureus USA300 pneumonia has been attributed to the PVL-associated release of cytotoxic components from PMN granules (5). In models of soft tissue infection, the importance ...

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Section: Discussionsupporting

confidence: 67%

Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

et al. 2011

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“…Addition of rHla to the extracellular medium of such cells induces elevations in [Ca 2ϩ ] i (14,50) and may increase membrane permeability for monovalent cations (31,58). This may directly or indirectly affect ciliary beat frequency, fluid and mucus secretion, or the release of proinflammatory cytokines and chemokines (7,11,15,33,39,43,51). These functional changes are supposed to represent defensive actions of the epithelial cells against the bacteria (32).…”

Section: Resultsmentioning

confidence: 99%

Staphylococcus aureusα-toxin-mediated cation entry depolarizes membrane potential and activates p38 MAP kinase in airway epithelial cells

Eiffler

Behnke

Ziesemer

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…This results in CD4 1 T-cell chemotaxis (135) and contributes to inflammation (136,137). The CXCR3 cytokines can exert direct antibacterial effects against gram-positive and gram-negative organisms (136,138).…”

Section: Cxcr3mentioning

confidence: 99%

Innate Immunity in the Respiratory Epithelium

Parker

Prince

2011

Am J Respir Cell Mol Biol

393

404

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The airway epithelium represents the first point of contact for inhaled foreign organisms. The protective arsenal of the airway epithelium is provided in the form of physical barriers and a vast array of receptors and antimicrobial compounds that constitute the innate immune system. Many of the known innate immune receptors, including the Toll-like receptors and nucleotide oligomerization domain-like receptors, are expressed by the airway epithelium, which leads to the production of proinflammatory cytokines and chemokines that affect microorganisms directly and recruit immune cells, such as neutrophils and T cells, to the site of infection. The airway epithelium also produces a number of resident antimicrobial proteins, such as lysozyme, lactoferrin, and mucins, as well as a swathe of cationic proteins. Dysregulation of the airway epithelial innate immune system is associated with a number of medical conditions that can result in compromised immunity and chronic inflammation of the lung. This review focuses on the innate immune capabilities of the airway epithelium and its role in protecting the lung from infection as well as the outcomes when its function is compromised.

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T Cell Chemotaxis and Chemokine Release afterStaphylococcus aureusInteraction with Polarized Airway Epithelium

Cited by 30 publications

References 36 publications

Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

Staphylococcus aureusα-toxin-mediated cation entry depolarizes membrane potential and activates p38 MAP kinase in airway epithelial cells

Innate Immunity in the Respiratory Epithelium

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T Cell Chemotaxis and Chemokine Release afterStaphylococcus aureusInteraction with Polarized Airway Epithelium

Cited by 30 publications

References 36 publications

Participation of CD11c + Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

Participation of CD11c + Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

Staphylococcus aureusα-toxin-mediated cation entry depolarizes membrane potential and activates p38 MAP kinase in airway epithelial cells

Innate Immunity in the Respiratory Epithelium

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Product

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Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung