Modulation of Systemic and Mucosal Immune Responses to Inhaled Ragweed Antigen in Experimentally Induced Infection with Respiratory Syncytial Virus Implication in Virally Induced Allergy

Leibovitz, E. E.; Freihorst, Joachim; Piedra, Pedro A.; Ogra, Pearay L.

doi:10.1159/000234615

Cited by 55 publications

(31 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The RSV G protein especially mounts an IgE response (33,34). Several investigators reported allergen-specific IgE enhancement in animals with prior RSV (35,36), influenza (37), or parainfluenza-3 viral (38) infection, suggesting that the virus-induced increase in allergen-specific IgE is possibly due to the facilitation of allergen uptake by virally damaged epithelial cells. It is likely that an increase in Df-specific IgE was not detected in the present study because mice were first sensitized and challenged with allergen and subsequently infected with RSV.…”

Section: Discussionmentioning

confidence: 99%

Recurrent Respiratory Syncytial Virus Infections in Allergen-Sensitized Mice Lead to Persistent Airway Inflammation and Hyperresponsiveness

Matsuse

Behera

Kumar

et al. 2000

The Journal of Immunology

View full text Add to dashboard Cite

Respiratory syncytial virus (RSV) infection is considered a risk factor for bronchial asthma; however, the synergy between allergen sensitization and RSV infection in the development of pulmonary inflammation and asthma has been controversial. In this study the effects of primary and recurrent RSV infection on allergic asthma were examined in a group of control, RSV-infected, Dermatophagoides farinae (Df) allergen-sensitized, and Df allergen-sensitized plus RSV-infected BALB/c mice. Primary RSV infection in Df-sensitized mice transiently increases airway responsiveness, which is accompanied by increases in eosinophilic infiltration, the expression of ICAM-1, and macrophage inflammatory protein-1α (MIP-1α) in the lung tissue. A secondary RSV infection persistently enhances airway responsiveness in Df-sensitized mice, with a concomitant increase in MIP-1α and RSV Ag load in lung tissues. Bulk cultures of thoracic lymph node mononuclear cells demonstrate that acute RSV infection augments both Th1- and Th2-like cytokines, whereas secondary and tertiary infections shift the cytokine profile in favor of the Th2-like cytokine response in Df-sensitized mice. The elevated total serum IgE level in the Df-sensitized mice persists following only RSV reinfection. Thus, recurrent RSV infections in Df-sensitized mice augment the synthesis of Th2-like cytokines, total serum IgE Abs, and MIP-1α, which are responsible for persistent airway inflammation and hyperresponsiveness, both of which are characteristics of asthma.

show abstract

Section: Discussionmentioning

confidence: 99%

Recurrent Respiratory Syncytial Virus Infections in Allergen-Sensitized Mice Lead to Persistent Airway Inflammation and Hyperresponsiveness

Matsuse

Behera

Kumar

et al. 2000

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…Experimentally, the phenomenon of allergen sensitization via the lung as a result of coincidental exposure to environmental "adjuvants" or infectious agents has also been previously described. Among the infectious factors that may contribute to permanent IgE sensitization are respiratory syncytial virus (RSV) (47)(48)(49)(50)(51), Rhinovirus (52,53), Bordetella pertussis (54 -57), and EBV. In addition, the ability of environmental factors to alter the development of IgE tolerance such as exposure to smoke, diesel particles, or ozone has been described (58,59).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Inhaled Antigen-Induced IgE Tolerance by Ongoing Th2 Responses in the Lung

Hurst

Seymour

Muchamuel

et al. 2001

The Journal of Immunology

View full text Add to dashboard Cite

The normal response to inhaled Ag is the absence of Ag-specific IgE and cytokine production to later Ag challenges. Although the mechanism of this aerosol-induced IgE tolerance is not completely understood, it may prevent sensitization to inhaled Ags, which could otherwise lead to allergy and asthma. We examined the consequences of ongoing Th1 and Th2 responses in the lungs of mice during OVA inhalation to mimic conditions that may subvert tolerance and lead to sensitization. We found that concurrent, secondary Th2 lung responses to keyhole limpet hemocyanin or primary responses to Nippostrongylus larvae or Asperigillus fumagatus extract prevented establishment of IgE tolerance to aerosolized OVA. Intranasal rIL-4 given before OVA aerosolization also prevented establishment of tolerance, whereas concurrent Th1 responses to influenza virus or Mycobacterium bovis bacillus Calmette-Guérin had no effect. However, once established, aerosol tolerance to OVA could not be completely broken by OVA rechallenge concurrent with a secondary Th2 response to keyhole limpet hemocyanin or A. fumagatus extract, or by intranasal rIL-4. These data suggest that the immune status of the lung of an individual may profoundly influence the initial response to inhaled Ag, and that aerosol-induced IgE tolerance may not be appropriately established in individuals undergoing concurrent, Th2-mediated responses to Ags or pathogens.

show abstract

“…The results suggested that RSV infection can enhance the development of sensitization and the magnitude of antibody responses to other inhaled allergens found concomitantly in the respiratory tract during acute infection [38,39].…”

Section: Infectionsmentioning

confidence: 94%

In 2532 Children we Report the Developmental Factors Influencing the Development of Atopic Diseases

Cantani¹

2017

Austin J Allergy

View full text Add to dashboard Cite

Allergic asthma and rhinitis, Atopic Dermatitis (AD), urticaria and gastrointestinal allergy, are common diseases of infants and children. It was recently estimated that 14% of children suffer from AD, 8% from food allergy, and 12% from asthma [1,2]. The cumulated incidence of these diseases in adolescents has been estimated between 25-35%, while the prevalence is about 20% [3]. The phenotypic expression of these illnesses varies extensively, being very mild in some cases, severe in many, and even life threatening in others. Specific IgE antibodies to foods and positive challenge tests to a number of food allergens are frequently present in children with these disorders. Cow's Milk (CM) appears to be the most common offending food both in gastrointestinal (vomiting, diarrhea, etc) and in cutaneous manifestations (urticaria and AD). About 0.5-7% of infants suffer from more or less adverse reactions to CM [4]. Babies particularly of atopic parents are at high risk of developing atopic diseases; therefore they are defined as at-risk babies [5][6][7].conditions. It has been known for centuries that heredity plays an important role in the development of atopy. A child with a negative family history still has about a 5-15% risk of developing atopy. However, children with a parental history of atopic disease are at higher risk for the development of atopic symptoms. It has been found that if one parent is affected, the chances of an offspring being affected vary between 20 and 40%. If both parents are affected the figure increases up to 40-60%, and 50-80% if both show the same allergic manifestations. The risk of atopy in children who have an allergic sibling ranges between 25 and 35% [3,10].The importance of genetic factors is also demonstrated by other data:(I) children with positive family history for atopy develop allergic symptoms earlier than those with a negative family history [11], (II) The higher the incidence the higher the number of affected subjects in the same family [3].Notable differences exist in the so-called predisposition to atopic diseases, and further study appears to be necessary to better delineate the role played by genetic factors in the development of such disorders.In many allergic patients total serum IgE levels are found to be elevated, and it has been shown that a high total serum IgE level in infants is often associated with the subsequent development of atopic symptoms. Therefore, it was proposed that the measurement of IgE by PRIST testing in infants or at birth would have a predictive value in the atopy development. Several investigators have demonstrated that the risk of developing atopic diseases was very high when the cord IgE level was above 0.5 IU/ml [5,8,9,12].Our data shows that a newborn can be considered at risk for atopy when the cord IgE level is above 0.8 IU/ml [5]. We have also shown that neonates of non atopic parents (0.032 + 0

show abstract

Modulation of Systemic and Mucosal Immune Responses to Inhaled Ragweed Antigen in Experimentally Induced Infection with Respiratory Syncytial Virus Implication in Virally Induced Allergy

Cited by 55 publications

References 6 publications

Recurrent Respiratory Syncytial Virus Infections in Allergen-Sensitized Mice Lead to Persistent Airway Inflammation and Hyperresponsiveness

Recurrent Respiratory Syncytial Virus Infections in Allergen-Sensitized Mice Lead to Persistent Airway Inflammation and Hyperresponsiveness

Modulation of Inhaled Antigen-Induced IgE Tolerance by Ongoing Th2 Responses in the Lung

In 2532 Children we Report the Developmental Factors Influencing the Development of Atopic Diseases

Contact Info

Product

Resources

About