Is histamine responsible for the symptoms of rhinovirus colds? a look at the inflammatory mediators following infection

Naclerio, R. M.; Proud, David; Kagey-Sobotka, A.; Lichtenstein, L M; Hendley, J. Owen; Gwaltney, Jr Jm

doi:10.1097/00006454-198803000-00031

Cited by 35 publications

(21 citation statements)

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“…Increases in nasal secretions are universal manifestations of infection, often accompanied by nasal blockage and sore throat and less often by constitutional symptoms. The genesis of a 'runny nose' is poorly understood and has been ascribed to the release of kinins [Naclerio et al, 1988] and other vasoactive substances such as leukotriene C4 [Skoner et al, 1995;Gentile et al, 2003]. The potent effects of the angiogenic factor VEGF on vascular permeability have been characterized and found to be more than a 1000-fold greater than histamine [Senger et al, 1990].…”

Section: Discussionmentioning

confidence: 99%

“…The genesis of classical cold symptoms such as rhinorhea, nasal blockage, sore throat and cough following infection is not defined but may be the result of kinin release and other vasoactive substances induced by rhinovirus [Naclerio et al, 1988]. However, initial rhinovirus infection occurs in the airway mucosa and release of other permeability factors from epithelial and fibroblast cells may explain the development of rhinorrhea at an early stage, usually within 48 hr [Grunberg and Sterk, 1999].…”

Section: Introductionmentioning

confidence: 99%

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Vascular endothelial growth factor induction by rhinovirus infection

et al. 2006

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Vascular participation manifested by a runny nose (rhinorrhea) is a prominent feature of the acute consequences of rhinovirus infection. Vascular endothelial growth factor (VEGF) is an angiogenic factor that also induces potent increases in vascular permeability; it is a candidate mediator of rhinorrhea in response to rhinovirus infection as well as contributing to enhanced vascular leakage in rhinovirus-linked asthma exacerbations. It has been shown that rhinovirus induces significant increases in both VEGF protein and mRNA in primary airway fibroblasts [Ghildyal et al. (2005): J Med Virol 75:608-615]. The current studies assessed VEGF responses to rhinovirus in primary culture airway epithelium, in epithelial and fibroblast cell lines and in rhinovirus-infected nasal secretions. Epithelial and fibroblast cells were infected with rhinovirus serotype 16 and VEGF protein and isoforms assessed by ELISA and RT-PCR, respectively. VEGF protein was released by both epithelial and fibroblast cell lines and primary airway epithelial cells in culture but was not increased following rhinovirus infection. PCR products coding for four or five of the six known VEGF isoforms were produced (121, 145, 165 and 183, and/or 189 amino acids) in cell lines and primary culture cells, but no specific isoform was linked to rhinovirus infection. Nasal VEGF was also measured in a cohort of asthmatics with verified rhinovirus and respiratory syncytial virus (RSV) infection. VEGF was not raised following rhinovirus infection alone, but was increased significantly if concomitant RSV infection was present. The data suggest that fibroblasts rather than the epithelium may play a key role in VEGF mediated vascular responses after rhinovirus infection. This may aid recruitment of inflammatory cells and contribute to airway inflammation and bronchial obstruction.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Vascular endothelial growth factor induction by rhinovirus infection

et al. 2006

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“…Early attempts to identify possible signaling molecules synthesized or released during a vURI focused on established mediators of the nasal allergic reaction and included histamine, bradykinin, and the prostaglandins, leukotrienes, and other arachidonic acid metabolites [1][2][3]27,28]. The usual format for these studies was daily monitoring for symptoms/signs and periodic assay of recovered nasal lavage fluids for suspected "mediators" in adults experimentally exposed to a "common cold" virus.…”

Section: Causalitymentioning

confidence: 99%

“…(Kant, 1781) A traditional method for studying the pathogenesis of upper respiratory diseases and their complications is the assay of secretions and/or other recovered fluids for chemicals that are expected to participate in the immune/ inflammatory process. For example, assays of nasal secretions/washings [1][2][3], sinus fluids [4], and middle ear effusions [5] for "classic" inflammatory mediators (eg, histamine, bradykinin, arachidonic acid metabolites) and, more recently, for intercellular signaling chemicals (eg, cytokines, chemokines) [6][7][8][9] have been performed by numerous laboratories, and the results related to extant symptom/sign expression. In turn, temporal correlations between signal (chemical) and response (symptom/sign) were often interpreted in terms of causal mediation and, therefore, as potential targets for pharmacologic modulation of the response.…”

Section: Introductionmentioning

confidence: 99%

Nasal cytokines as mediators of illness during the common cold

Doyle

Skoner

Gentile

2005

Curr Allergy Asthma Rep

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Identification of a pharmacologically targeted mediator of the common cold is a desirable, but, to date, elusive goal of current research. The roles of various mediators, such as histamine, leukotrienes, bradykinin, and, more recently, chemokines and cytokines, in the pathophysiology and development of complications of the common cold are the subject of previous and current investigations. Establishing causality of a mediator in the common cold has been difficult for a number of reasons, including the limitations of our research tools and protocols and the complexity of the inflammatory and immune pathways that participate during the common cold. The available evidence for mediation of the common cold is the subject of this manuscript.

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“…EV RT infections cause transient, benign symptoms, such as rhinorrhea, sneezing, and sore throat, but they are major factors in the exacerbation of asthma (28,35) and chronic obstructive pulmonary disease (COPD) (37,38). Curiously, viral replication is modest and host cell destruction in the RT is absent (21,44), indicating a role of host inflammatory reactions rather than overt tissue damage in pathogenesis (33,34). The significant public health impact of EV RT infections inspired many efforts to develop animal models.…”

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confidence: 99%

Adaptation of an ICAM-1-Tropic Enterovirus to the Mouse Respiratory Tract

Wang

Dobrikova

Goetz

et al. 2011

J Virol

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Respiratory tract (RT) infections by members of the enterovirus (EV) genus of the Picornaviridae family are the most frequent cause for the common cold and a major factor in the exacerbation of chronic pulmonary diseases. The lack of a practical small-animal model for these infections has obstructed insight into pathogenic mechanisms of the common cold and their role in chronic RT illness and has hampered preclinical evaluation of antiviral strategies. Despite significant efforts, it has been difficult to devise rodent models that exhibit viral replication in the RT. This is due mainly to well-known intracellular host restrictions of EVs with RT tropism in rodent cells. We report the evolution of variants of the common-cold-causing coxsackievirus A21, an EV with tropism for the human intercellular adhesion molecule 1 (hICAM-1), through serial passage in the lungs of mice transgenic for the hICAM-1 gene. This process was accompanied by multiple changes in the viral genome, suggesting exquisite adaptation of hICAM-1-tropic enteroviruses to the specific growth conditions within the RT. In vivo mouse RT-adapted, variant coxsackievirus A21 exhibited replication competence in the lungs of hICAM-1 transgenic mice, providing a basis for unraveling EV-host interactions in the mouse RT.The common cold (acute nasopharyngitis) is a frequent ailment, primarily of viral etiology, recognized since antiquity. The incidence in adults and children ranges from 2 to 4 and 6 to 8 cases, respectively, per person per year. The economic impact of viral, noninfluenza respiratory tract (RT) infections has been estimated at ϳ$40 billion/year in the United States alone (16). A majority of viral infections are due to members of the enterovirus (EV) genus of the Picornaviridae family recognizing hICAM-1 as a receptor (20,39,40). These comprise 88 major-group human rhinoviruses (HRVs) and coxsackievirus A (CAV) serotypes 1, 11, 13, 15, and 17 to 24. EV RT infections cause transient, benign symptoms, such as rhinorrhea, sneezing, and sore throat, but they are major factors in the exacerbation of asthma (28, 35) and chronic obstructive pulmonary disease (COPD) (37, 38). Curiously, viral replication is modest and host cell destruction in the RT is absent (21, 44), indicating a role of host inflammatory reactions rather than overt tissue damage in pathogenesis (33, 34). The significant public health impact of EV RT infections inspired many efforts to develop animal models. Since natural susceptibility is restricted to higher primates (12), these approaches were based on adapting EVs to rodents. HRVs that use the lowdensity lipoprotein receptor (LDL-R) for host cell entry spontaneously infect mouse L fibroblasts (47) and exhibit very modest replication in wild-type (wt) BALB/c mice (46). This suggests that these viruses either use the murine LDL-R or another murine cell surface molecule for host cell attachment and entry. More targeted, recent efforts focused on supplying authentic human receptors, e.g., with mice transgenic for the hICAM-1 gene (...

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Is histamine responsible for the symptoms of rhinovirus colds? a look at the inflammatory mediators following infection

Cited by 35 publications

References 0 publications

Vascular endothelial growth factor induction by rhinovirus infection

Vascular endothelial growth factor induction by rhinovirus infection

Nasal cytokines as mediators of illness during the common cold

Adaptation of an ICAM-1-Tropic Enterovirus to the Mouse Respiratory Tract

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