Nasal mucosal temperature during respiration

Lindemann, Jörg; Liu, Richard; Rettinger, Gerhard; Keck, Tilman

doi:10.1046/j.1365-2273.2002.00544.x

Cited by 198 publications

(178 citation statements)

References 26 publications

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“…The surface temperatures of the human respiratory tract range from 32 Ϯ 0.05°C in the proximal large airways (i.e., nasal and tracheal) to 37°C in the smaller distal airways (i.e., bronchioles) (19,23). Previously, a correlation was observed between the high-transmissibility phenotype of influenza viruses in ferrets and their ability to replicate efficiently at the lower temperature of 33°C (36).…”

Section: Resultsmentioning

confidence: 99%

The 2009 Pandemic H1N1 and Triple-Reassortant Swine H1N1 Influenza Viruses Replicate Efficiently but Elicit an Attenuated Inflammatory Response in Polarized Human Bronchial Epithelial Cells

Zeng

Pappas

Katz

et al. 2011

J Virol

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Section: Resultsmentioning

confidence: 99%

The 2009 Pandemic H1N1 and Triple-Reassortant Swine H1N1 Influenza Viruses Replicate Efficiently but Elicit an Attenuated Inflammatory Response in Polarized Human Bronchial Epithelial Cells

Zeng

Pappas

Katz

et al. 2011

J Virol

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“…The upper nasopharynx, particularly the nasal mucosa, is one of the primary colonization sites for B. bronchiseptica. The temperature in this area in mammals is measured to be between 30 and 34°C (19). Temperature is an environmental signal that can mediate Bvg regulation, and this range of temperature would modulate the bacteria into the Bvg i phase.…”

Section: Discussionmentioning

confidence: 99%

The Bvg Virulence Control System Regulates Biofilm Formation in Bordetella bronchiseptica

2004

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؉ phase encode known virulence factors, including adhesins such as filamentous hemagglutinin (FHA) and fimbriae, as well as toxins such as the bifunctional adenylate cyclase/hemolysin (ACY). Previous studies showed that in the Bvg i phase, FHA and fimbriae continue to be expressed, but ACY expression is significantly downregulated. In this report, we determine that Bordetella bronchiseptica can form biofilms in vitro and that the generation of biofilm is maximal in the Bvg i phase. We show that FHA is required for maximal biofilm formation and that fimbriae may also contribute to this phenotype. However, expression of ACY inhibits biofilm formation, most likely via interactions with FHA. Therefore, the coordinated regulation of adhesins and ACY expression leads to maximal biofilm formation in the Bvg i phase in B. bronchiseptica.Bordetella pertussis, Bordetella parapertussis, and Bordetella bronchiseptica are closely related gram-negative coccobacilli that colonize the upper respiratory tract of mammals. B. pertussis and most B. parapertussis strains are obligate human pathogens that usually cause acute respiratory diseases. B. bronchiseptica has a much broader host range and is considered to be representative of the evolutionary progenitor of all Bordetella spp. (10, 27). It naturally infects many laboratory animals, including mice, rats, and rabbits, and thus serves as an ideal model for studying bacterial pathogenesis in a natural infection setting. Although B. bronchiseptica has been associated with various respiratory diseases, infection by this organism generally leads to chronic and asymptomatic colonization in the host. This lifestyle indicates that the bacteria employ specific mechanisms to counteract host immune responses and also implies successful interactions with other commensal bacteria commonly found in the upper respiratory tract.

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“…Unlike human influenza viruses, which replicate efficiently in respiratory tracts where the temperatures range from 32°C in the upper respiratory tract to 37°C in lower respiratory tract (34,35), avian influenza viruses have adapted to replicate at the higher temperatures, 40 to 41°C, of the avian enteric tract (36). The upper respiratory tract provides a large surface area of susceptible cells and is usually the initial site of infection and likely the predominant site of influenza virus replication in mammalian species (37).…”

Section: Figmentioning

confidence: 99%

Pathogenesis and Transmission of Novel Highly Pathogenic Avian Influenza H5N2 and H5N8 Viruses in Ferrets and Mice

Pulit-Penaloza

Sun

Creager

et al. 2015

J Virol

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A novel highly pathogenic avian influenza (HPAI) H5N8 virus, first detected in January 2014 in poultry and wild birds in South Korea, has spread throughout Asia and Europe and caused outbreaks in Canada and the United States by the end of the year. The spread of H5N8 and the novel reassortant viruses, H5N2 and H5N1 (H5Nx), in domestic poultry across multiple states in the United States pose a potential public health risk. To evaluate the potential of cross-species infection, we determined the pathogenicity and transmissibility of two Asian-origin H5Nx viruses in mammalian animal models. The newly isolated H5N2 and H5N8 viruses were able to cause severe disease in mice only at high doses. Both viruses replicated efficiently in the upper and lower respiratory tracts of ferrets; however, the clinical symptoms were generally mild, and there was no evidence of systemic dissemination of virus to multiple organs. Moreover, these influenza H5Nx viruses lacked the ability to transmit between ferrets in a direct contact setting. We further assessed viral replication kinetics of the novel H5Nx viruses in a human bronchial epithelium cell line, Calu-3. Both H5Nx viruses replicated to a level comparable to a human seasonal H1N1 virus, but significantly lower than a virulent Asian-lineage H5N1 HPAI virus. Although the recently isolated H5N2 and H5N8 viruses displayed moderate pathogenicity in mammalian models, their ability to rapidly spread among avian species, reassort, and generate novel strains underscores the need for continued risk assessment in mammals. O n 16 December 2014, the U.S. Department of Agriculture (USDA) confirmed the presence of a novel highly pathogenic avian influenza (HPAI) H5N8 virus in a captive gyrfalcon and H5N2 virus in a northern pintail duck from Whatcom County, Washington (1). This represented the first appearance of HPAI H5 virus in the United States since 2004 when H5N2 subtype virus was confirmed on a poultry farm in Texas (2). HPAI H5N8 viruses were first reported in duck farms in eastern China in 2010, and in early 2014 a novel reassortant H5N8 virus was detected in poultry in South Korea (3-5). The novel virus, belonging to Eurasian lineage clade 2.3.4.4 (formerly clade 2.3.4.6), subsequently spread to China, Japan, and five countries in Europe (6, 7). In November 2014, the virus was detected on chicken and turkey farms in British Columbia, Canada, followed by Washington State, USA, the following month (8). The novel H5N8 viruses continue to spread to multiple regions and have been found in three North America flyways (Pacific, Central, and Mississippi), where wild-bird migrations occur (USDA, Animal and Plant Health Inspection Service [http://www.aphis.usda.gov]). In addition, genetic reassortment with circulating North American avian influenza viruses has resulted in novel HPAI viruses, including H5N2 and H5N1 subtypes. These novel reassortant viruses carry a Eurasian-origin hemagglutinin (HA) gene genetically related to H5N8 viruses detected in South Korea in 2014 and the neura...

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Nasal mucosal temperature during respiration

Cited by 198 publications

References 26 publications

The 2009 Pandemic H1N1 and Triple-Reassortant Swine H1N1 Influenza Viruses Replicate Efficiently but Elicit an Attenuated Inflammatory Response in Polarized Human Bronchial Epithelial Cells

The 2009 Pandemic H1N1 and Triple-Reassortant Swine H1N1 Influenza Viruses Replicate Efficiently but Elicit an Attenuated Inflammatory Response in Polarized Human Bronchial Epithelial Cells

The Bvg Virulence Control System Regulates Biofilm Formation in Bordetella bronchiseptica

Pathogenesis and Transmission of Novel Highly Pathogenic Avian Influenza H5N2 and H5N8 Viruses in Ferrets and Mice

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