Physiologic Cold Shock Increases Adherence of<i>Moraxella catarrhalis</i>to and Secretion of Interleukin 8 in Human Upper Respiratory Tract Epithelial Cells

Spaniol, Violeta; Troller, Rolf; Aebi, Christoph

doi:10.1086/644640

Cited by 25 publications

(32 citation statements)

References 42 publications

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“…In addition, children of 3~5 y old are in the nursery period, the susceptible environment of kindergartens and immune function which have not been well developed yet cause it prone to bacterial infection of respiratory tract. In all age groups, detection rate of SP come first, especially in the age group 3~5 y old, it was the highest and the lowest in <6 months group, which were basically consistent with the reports from Cai et al [19] and Sun et al [21][22][23]. Previous reports have suggested that HI and E. coli infections are mainly seen in children under 1 y old [20,23,24].…”

Section: Resultssupporting

confidence: 89%

The characteristics of bacterial pathogens in 15000 cases of children with respiratory tract infection in Eastern area

Guiting¹,

Wang²,

Jiang³

et al. 2018

biomedicalresearch

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Section: Resultssupporting

confidence: 89%

The characteristics of bacterial pathogens in 15000 cases of children with respiratory tract infection in Eastern area

Guiting¹,

Wang²,

Jiang³

et al. 2018

biomedicalresearch

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“…The M. catarrhalis lipooligosaccharides (LOS) (68) and the outer membrane protein UspA1 might be involved in stimulating the secretion of IL-8 in vitro (57), and MID/Hag might be involved in B-cell activation (47,67). Importantly, serum samples from COPD patients who had recently cleared M. catarrhalis infection are reactive to M. catarrhalis LOS (53) and MID/Hag (40), indicating that M. catarrhalis extracellular components may contribute to the production of inflammatory disease.…”

Section: Figmentioning

confidence: 99%

Bacterium-Generated Nitric Oxide Hijacks Host Tumor Necrosis Factor Alpha Signaling and Modulates the Host Cell Cycle In Vitro

Mocca

Wang

2012

J Bacteriol

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In mammalian cells, nitric oxide (NO·) is an important signal molecule with concentration-dependent and often controversial functions of promoting cell survival and inducing cell death. An inducible nitric oxide synthase (iNOS) in various mammalian cells produces higher levels of NO· from L-arginine upon infections to eliminate pathogens. In this study, we reveal novel pathogenic roles of NO· generated by bacteria in bacterium-host cell cocultures using Moraxella catarrhalis, a respiratory tract disease-causing bacterium, as a biological producer of NO·. We recently demonstrated that M. catarrhalis cells that express the nitrite reductase (AniA protein) can produce NO· by reducing nitrite. Our study suggests that, in the presence of pathophysiological levels of nitrite, this opportunistic pathogen hijacks host cell signaling and modulates host gene expression through its ability to produce NO· from nitrite. Bacterium-generated NO· significantly increases the secretion of tumor necrosis factor alpha (TNF-␣) and modulates the expression of apoptotic proteins, therefore triggering host cell programmed death partially through TNF-␣ signaling. Furthermore, our study reveals that bacterium-generated NO· stalls host cell division and directly results in the death of dividing cells by reducing the levels of an essential regulator of cell division. This study provides unique insight into why NO· may exert more severe cytotoxic effects on fast growing cells, providing an important molecular basis for NO·-mediated pathogenesis in infections and possible therapeutic applications of NO·-releasing molecules in tumorigenesis. This study strongly suggests that bacterium-generated NO· can play important pathogenic roles during infections. In mammalian cells, nitric oxide (NO·) is a highly reactive and diffusible signaling molecule that plays key roles in modulating both physiological and pathological processes, such as immune response, cell survival, and cell death (reviewed in references 8 and 36). The diverse functions of NO· are often determined by its concentration or its source of production. Low levels of endogenous NO· are produced from L-arginine by constitutively expressed nitric oxide synthase in neuronal cells (nNOS, also known as NOS1) and endothelial cells (eNOS, also known as NOS3) to mediate normal physiological processes. Higher levels of NO· can be produced by an inducible nitric oxide synthase (iNOS, also known as NOS2) in different cell types, but mainly in macrophages, upon infection to kill pathogens (reviewed in reference 9). The higher levels of NO· produced by iNOS have been implicated in various human inflammatory diseases and neurodegenerative diseases (reviewed in references 9 and 12) and in chronic inflammation-related tumorigenesis (18, 33). Recent studies have also shown that chemical-generated higher levels of exogenous NO· can induce tumor cell apoptosis in vitro and in animal studies (37; reviewed in reference 1), raising interests in therapeutic exploration of NO·-releasing reagents as antitumor...

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“…The ability of M. catarrhalis to adhere to and invade human Detroit 562 epithelial cells in vitro was measured as described previously (13,27,28). Each strain was analyzed in triplicate in each experiment.…”

Section: Methodsmentioning

confidence: 99%

“…Such rapid variation of temperature induces adaptive events in the residential upper respiratory tract flora that may contribute to the transition from asymptomatic colonization to infection. Our previous in vitro studies demonstrated that a 26°C cold shock upregulates the expression of important virulence traits, such as adherence to epithelial cells, iron acquisition, complement resistance, and immune evasion (12)(13)(14).Adaptive resistance also involves a temporary increase in the ability of a bacterium to survive exposure to antimicrobials due to alterations in gene/protein expression as a result of an environmental trigger, e.g., temperature, stress, nutrient conditions, or subinhibitory levels of the antibiotics themselves (15). One of the main antimicrobial resistance strategies of bacteria is altered porin expression to limit intracellular access of antibiotics.…”

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confidence: 99%

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Moraxella catarrhalis AcrAB-OprM Efflux Pump Contributes to Antimicrobial Resistance and Is Enhanced during Cold Shock Response

Spaniol

Bernhard

Aebi

2015

Antimicrob Agents Chemother

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bMoraxella catarrhalis is a common pathogen of the human respiratory tract. Multidrug efflux pumps play a major role in antibiotic resistance and virulence in many Gram-negative organisms. In the present study, the role of the AcrAB-OprM efflux pump in antibiotic resistance was investigated by constructing mutants that lack the acrA, acrB, and oprM genes in M. catarrhalis strain O35E. We observed a moderate (1.5-fold) decrease in the MICs of amoxicillin and cefotaxime and a marked (4.7-fold) decrease in the MICs of clarithromycin for acrA, acrB, and oprM mutants in comparison with the wild-type O35E strain. Exposure of the M. catarrhalis strains O35E and 300 to amoxicillin triggered an increased transcription of all AcrAB-OprM pump genes, and exposure of strains O35E, 300, and 415 to clarithromycin enhanced the expression of acrA and oprM mRNA. Inactivation of the AcrAB-OprM efflux pump genes demonstrated a decreased ability to invade epithelial cells compared to the parental strain, suggesting that acrA, acrB, and oprM are required for efficient invasion of human pharyngeal epithelial cells. Cold shock increases the expression of AcrAB-OprM efflux pump genes in all three M. catarrhalis strains tested. Increased expression of AcrAB-OprM pump genes after cold shock leads to a lower accumulation of Hoechst 33342 (H33342), a substrate of AcrABOprM efflux pumps, indicating that cold shock results in increased efflux activity. In conclusion, the AcrAB-OprM efflux pump appears to play a role in the antibiotic resistance and virulence of M. catarrhalis and is involved in the cold shock response. Moraxella catarrhalis colonizes the mucosal surface of the human nasopharynx and is a major cause of acute otitis media in children and of exacerbations of chronic obstructive pulmonary disease in adults (1-4). The proportion of cases of acute otitis media caused by M. catarrhalis varies between 5% and 20%, with recent studies showing a relative increase in M. catarrhalis-caused otitis media since the introduction of routine infant immunization with the pneumococcal conjugate vaccine (2, 4-6). Furthermore, clinical studies revealed that the prevalence of pharyngeal colonization and respiratory tract infections caused by M. catarrhalis displays seasonal variation and increases in winter (7-10). The human nasopharyngeal flora is recurrently exposed to rapid downshifts of environmental temperature. Breathing cold air (e.g., Ϫ1°C at 10 to 20 liters/min) reduces the nasopharyngeal temperature from 34°C at room temperature to about 26°C within several minutes and for extended periods (11). Such rapid variation of temperature induces adaptive events in the residential upper respiratory tract flora that may contribute to the transition from asymptomatic colonization to infection. Our previous in vitro studies demonstrated that a 26°C cold shock upregulates the expression of important virulence traits, such as adherence to epithelial cells, iron acquisition, complement resistance, and immune evasion (12)(13)(14).Adaptive resistance also...

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Physiologic Cold Shock Increases Adherence ofMoraxella catarrhalisto and Secretion of Interleukin 8 in Human Upper Respiratory Tract Epithelial Cells

Cited by 25 publications

References 42 publications

The characteristics of bacterial pathogens in 15000 cases of children with respiratory tract infection in Eastern area

The characteristics of bacterial pathogens in 15000 cases of children with respiratory tract infection in Eastern area

Bacterium-Generated Nitric Oxide Hijacks Host Tumor Necrosis Factor Alpha Signaling and Modulates the Host Cell Cycle In Vitro

Moraxella catarrhalis AcrAB-OprM Efflux Pump Contributes to Antimicrobial Resistance and Is Enhanced during Cold Shock Response

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