The identification of response regulators of<i>Branhamella catarrhalis</i>using PCR

Mibus, Deborah J.; Mee, Brian; McGregor, Karen F.; Garbin, Christine D.; Chang, Barbara J.

doi:10.1111/j.1574-695x.1998.tb01225.x

Cited by 4 publications

(1 citation statement)

References 13 publications

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“…More recently, the ability of reduced temperature to influence the expression of numerous different M. catarrhalis gene products was reported (30), and small regulons controlled by the OxyR and NsrR proteins have been described (31,32). The likely presence of two-component signal transduction systems in M. catarrhalis was first noted in a PCR-based study which detected the presence of a gene encoding an OmpR family member that most closely resembled the PhoB response regulator of Pseudomonas aeruginosa (33). Analysis of the nucleotide sequence of the genome of M. catarrhalis ATCC 43617 (34) indicated the presence of at least four different two-component systems, a finding verified by subsequent analysis of the genomes of M. catarrhalis BBH18 (35) and 10 other M. catarrhalis strains (36,37).…”

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A Moraxella catarrhalis Two-Component Signal Transduction System Necessary for Growth in Liquid Media Affects Production of Two Lysozyme Inhibitors

et al. 2015

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There are a paucity of data concerning gene products that could contribute to the ability of Moraxella catarrhalis to colonize the human nasopharynx. Inactivation of a gene (mesR) encoding a predicted response regulator of a two-component signal transduction system in M. catarrhalis yielded a mutant unable to grow in liquid media. This mesR mutant also exhibited increased sensitivity to certain stressors, including polymyxin B, SDS, and hydrogen peroxide. Inactivation of the gene (mesS) encoding the predicted cognate sensor (histidine) kinase yielded a mutant with the same inability to grow in liquid media as the mesR mutant. DNA microarray and real-time reverse transcriptase PCR analyses indicated that several genes previously shown to be involved in the ability of M. catarrhalis to persist in the chinchilla nasopharynx were upregulated in the mesR mutant. Two other open reading frames upregulated in the mesR mutant were shown to encode small proteins (LipA and LipB) that had amino acid sequence homology to bacterial adhesins and structural homology to bacterial lysozyme inhibitors. Inactivation of both lipA and lipB did not affect the ability of M. catarrhalis O35E to attach to a human bronchial epithelial cell line in vitro. Purified recombinant LipA and LipB fusion proteins were each shown to inhibit human lysozyme activity in vitro and in saliva. A lipA lipB deletion mutant was more sensitive than the wild-type parent strain to killing by human lysozyme in the presence of human apolactoferrin. This is the first report of the production of lysozyme inhibitors by M. catarrhalis. Moraxella catarrhalis is a Gram-negative coccobacillus that can cause disease in both the upper and lower respiratory tracts of humans (1). In infants and young children, this bacterium is a significant cause of acute otitis media (i.e., middle ear infection) (2-4). In adults, M. catarrhalis can cause infectious exacerbations of chronic obstructive pulmonary disease (COPD) (5-7) and is likely responsible for approximately 4 million exacerbations of COPD annually in the United States (6). The latter disease has global significance because it has been predicted that by 2020, COPD will become the third leading cause of death worldwide (reviewed in reference 8). In addition, M. catarrhalis can cause sinusitis, pneumonia, and, more rarely, bacteremia (1, 9).M. catarrhalis colonization of the human nasopharynx is apparently asymptomatic and, at least in infancy, can be correlated with an increased risk of otitis media (10). In this anatomic niche, M. catarrhalis likely forms a biofilm, together with the normal bacterial flora of the nasopharynx (11, 12). Once established in the nasopharynx, this bacterium can spread to the middle ear (causing otitis media) or to the lower respiratory tract (resulting in an infectious exacerbation of COPD). A number of putative M. catarrhalis colonization or virulence factors have been described in the past decade (13-20), but identification of those bacterial gene products that are truly essential for nasop...

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