Intragastric and Intranasal Administration ofLactobacillus paracaseiNCC2461 Modulates Allergic Airway Inflammation in Mice

Introduction. Preclinical and clinical evidences for a role of oral probiotics in the management of allergic diseases are emerging.Aim. We aimed at testing the immunomodulatory effects of intranasalversusintragastric administration ofLactobacillus paracaseiNCC2461 in a mouse model of allergic airway inflammation and the specificity of different probiotics by comparingL. paracaseiNCC2461 toLactobacillus plantarumNCC1107.Methods.L. paracaseiNCC2461 orL. plantarumNCC1107 strains were administered either intragastrically (NCC2461) or intranasally (NCC2461 or NCC1107) to OVA-sensitized mice challenged with OVA aerosols. Inflammatory cell recruitment into BALF, eotaxin and IL-5 production in the lungs were measured.Results. IntranasalL. paracaseiNCC2461 efficiently protected sensitized mice upon exposure to OVA aerosols in a dose-dependent manner as compared to control mice. Inflammatory cell number, eotaxin and IL-5 were significantly reduced in BALF. Intranasal supplementation ofL. paracaseiNCC2461 was more potent than intragastric application in limiting the allergic response and possibly linked to an increase in T regulatory cells in the lungs. Finally, intranasalL. plantarumNCC1107 reduced total and eosinophilic lung inflammation, but increased neutrophilia and macrophages infiltration.Conclusion. A concerted selection of intervention schedule, doses, and administration routes (intranasal versus intragastric) may markedly contribute to modulate airway inflammation in a probiotic strain-specific manner.

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Faculty Opinions recommendation of Regulatory B cells prevent and reverse allergic airway inflammation via FoxP3-positive T regulatory cells in a murine model.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.4502961.4359059 ◽

2010 ◽

Author(s):

Min Lu

Keyword(s):

B Cells ◽

Airway Inflammation ◽

Murine Model ◽

T Regulatory Cells ◽

Allergic Airway Inflammation ◽

Regulatory Cells ◽

Regulatory B Cells

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The transfer of maternal antigen-specific IgG regulates the development of allergic airway inflammation early in life in an FcRn-dependent manner

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2010.03.170 ◽

2010 ◽

Vol 395 (2) ◽

pp. 238-243 ◽

Cited By ~ 22

Author(s):

Kyosuke Nakata ◽

Kazuyuki Kobayashi ◽

Yumiko Ishikawa ◽

Masatsugu Yamamoto ◽

Yasuhiro Funada ◽

...

Keyword(s):

Airway Inflammation ◽

Allergic Airway Inflammation ◽

Dependent Manner ◽

Specific Igg

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Diabetes Downregulates Allergen-Induced Airway Inflammation in Mice

Mediators of Inflammation ◽

10.1155/2018/6150843 ◽

2018 ◽

Vol 2018 ◽

pp. 1-11 ◽

Cited By ~ 4

Author(s):

Vinicius F. Carvalho ◽

Emiliano O. Barreto ◽

Ana Carolina S. Arantes ◽

Magda F. Serra ◽

Tatiana Paula T. Ferreira ◽

...

Keyword(s):

Airway Inflammation ◽

Bronchoalveolar Lavage Fluid ◽

Allergic Airway Inflammation ◽

Allergic Diseases ◽

Lavage Fluid ◽

Airway Hyperreactivity ◽

Eosinophil Infiltration ◽

Mucus Production ◽

Diabetes Induction

Previous studies described that allergic diseases, including asthma, occur less often than expected in patients with type 1 diabetes. Here, we investigated the influence of diabetes on allergic airway inflammation in a model of experimental asthma in mice. Diabetes was induced by intravenous injection of alloxan into 12 h-fasted A/J mice, followed by subcutaneous sensitization with ovalbumin (OVA) and aluminum hydroxide (Al(OH)3), on days 5 and 19 after diabetes induction. Animals were intranasally challenged with OVA (25 μg), from day 24 to day 26. Alloxan-induced diabetes significantly attenuated airway inflammation as attested by the lower number of total leukocytes in the bronchoalveolar lavage fluid, mainly neutrophils and eosinophils. Suppression of eosinophil infiltration in the peribronchiolar space and generation of eosinophilotactic mediators, such as CCL-11/eotaxin, CCL-3/MIP-1α, and IL-5, were noted in the lungs of diabetic sensitized mice. In parallel, reduction of airway hyperreactivity (AHR) to methacholine, mucus production, and serum IgE levels was also noted under diabetic conditions. Our findings show that alloxan diabetes caused attenuation of lung allergic inflammatory response in A/J mice, by a mechanism possibly associated with downregulation of IgE antibody production.

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Changes in Pulmonary Function and Parasite Burden in Rats Infected with Strongyloides venezuelensis Concomitant with Induction of Allergic Airway Inflammation

Infection and Immunity ◽

10.1128/iai.71.5.2607-2614.2003 ◽

2003 ◽

Vol 71 (5) ◽

pp. 2607-2614 ◽

Cited By ~ 39

Author(s):

Deborah Negrão-Corrêa ◽

Micheline R. Silveira ◽

Cynthia M. Borges ◽

Danielle G. Souza ◽

Mauro M. Teixeira

Keyword(s):

Airway Inflammation ◽

Mutual Influence ◽

Pulmonary Inflammation ◽

Allergic Airway Inflammation ◽

Parasite Burden ◽

Allergic Diseases ◽

Lavage Fluid ◽

Eosinophil Infiltration ◽

Asthmatic Patients ◽

Strongyloides Venezuelensis

ABSTRACT The prevalence of allergic diseases such as asthma has increased markedly over the past few decades. To evaluate the possible mutual influence of helminth infection and allergy, the combined effects of experimental allergic airway inflammation and infection with Strongyloides venezuelensis on various parasitological and inflammatory indices were evaluated in the rat. A challenge of immunized rats with aerosolized ovalbumin (OVA) resulted in eosinophilic inflammation that peaked 48 h after the challenge and was accompanied by airway hyperresponsiveness (AHR) to an intravenous acetylcholine challenge. S. venezuelensis infection concomitant with an OVA challenge of immunized rats resulted in prolonged pulmonary inflammation with increased eosinophil infiltration in bronchoalveolar lavage fluid but not in the lung tissue. These rats also showed a significant parasite burden reduction, especially during parasite migration through the lungs. However, the fecundity rates of worms that reached the intestine were similar in allergic and nonallergic animals. Despite airway inflammation, the increased responsiveness of the airways in the experimental asthma model was suppressed during parasite migration through the lungs (2 days). In contrast, parasite-induced AHR was unchanged 5 days after infection in immunized and challenged rats. In conclusion, infection with S. venezuelensis interfered with the onset of AHR following an antigen challenge of immunized rats. The ability of parasites to switch off functional airway responses is therapeutically relevant because we may learn from parasites how to modulate lung function and, hence, the AHR characteristic of asthmatic patients.

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Allergic Airway Inflammation Decreases Lung Bacterial Burden following Acute Klebsiella pneumoniae Infection in a Neutrophil- and CCL8-Dependent Manner

Infection and Immunity ◽

10.1128/iai.00035-14 ◽

2014 ◽

Vol 82 (9) ◽

pp. 3723-3739 ◽

Cited By ~ 16

Author(s):

Daniel E. Dulek ◽

Dawn C. Newcomb ◽

Kasia Goleniewska ◽

Jaqueline Cephus ◽

Weisong Zhou ◽

...

Keyword(s):

Klebsiella Pneumoniae ◽

Airway Inflammation ◽

Ex Vivo ◽

Allergic Airway Inflammation ◽

Dependent Manner ◽

Content Type ◽

Th2 Cytokine ◽

Interleukin 17A ◽

Th17 Cytokines

ABSTRACTThe Th17 cytokines interleukin-17A (IL-17A), IL-17F, and IL-22 are critical for the lung immune response to a variety of bacterial pathogens, includingKlebsiella pneumoniae. Th2 cytokine expression in the airways is a characteristic feature of asthma and allergic airway inflammation. The Th2 cytokines IL-4 and IL-13 diminishex vivoandin vivoIL-17A protein expression by Th17 cells. To determine the effect of IL-4 and IL-13 on IL-17-dependent lung immune responses to acute bacterial infection, we developed a combined model in which allergic airway inflammation and lung IL-4 and IL-13 expression were induced by ovalbumin sensitization and challenge prior to acute lung infection withK. pneumoniae. We hypothesized that preexisting allergic airway inflammation decreases lung IL-17A expression and airway neutrophil recruitment in response to acuteK. pneumoniaeinfection and thereby increases the lungK. pneumoniaeburden. As hypothesized, we found that allergic airway inflammation decreased the number ofK. pneumoniae-induced airway neutrophils and lung IL-17A, IL-17F, and IL-22 expression. Despite the marked reduction in postinfection airway neutrophilia and lung expression of Th17 cytokines, allergic airway inflammation significantly decreased the lungK. pneumoniaeburden and postinfection mortality. We showed that the decreased lungK. pneumoniaeburden was independent of IL-4, IL-5, and IL-17A and partially dependent on IL-13 and STAT6. Additionally, we demonstrated that the decreased lungK. pneumoniaeburden associated with allergic airway inflammation was both neutrophil and CCL8 dependent. These findings suggest a novel role for CCL8 in lung antibacterial immunity againstK. pneumoniaeand suggest new mechanisms of orchestrating lung antibacterial immunity.

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High-dose but not low-dose mainstream cigarette smoke suppresses allergic airway inflammation by inhibiting T cell function

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00392.2007 ◽

2008 ◽

Vol 295 (3) ◽

pp. L412-L421 ◽

Cited By ~ 33

Author(s):

Thomas H. Thatcher ◽

Randi P. Benson ◽

Richard P. Phipps ◽

Patricia J. Sime

Keyword(s):

T Cell ◽

Airway Inflammation ◽

Cigarette Smoke ◽

Significant Risk ◽

Allergic Airway Inflammation ◽

High Dose ◽

Dependent Manner ◽

Exposure System ◽

Specific Antibodies ◽

Mainstream Cigarette Smoke

Epidemiological studies have identified childhood exposure to environmental tobacco smoke as a significant risk factor for the onset and exacerbation of asthma, but studies of smoking in adults are less conclusive, and mainstream cigarette smoke (MCS) has been reported to both enhance and attenuate allergic airway inflammation in animal models. We sensitized mice to ovalbumin (OVA) and exposed them to MCS in a well-characterized exposure system. Exposure to MCS (600 mg/m3 total suspended particulates, TSP) for 1 h/day suppresses the allergic airway response, with reductions in eosinophilia, tissue inflammation, goblet cell metaplasia, IL-4 and IL-5 in bronchoalveolar lavage (BAL) fluid, and OVA-specific antibodies. Suppression is associated with a loss of antigen-specific proliferation and cytokine production by T cells. However, exposure to a lower dose of MCS (77 mg/m3 TSP) had no effect on the number of BAL eosinophils or OVA-specific antibodies. This is the first report to demonstrate, using identical smoking methodologies, that MCS inhibits immune responses in a dose-dependent manner and may explain the observation that, although smoking provokes a systemic inflammatory response, it also inhibits T cell-mediated responses involved in a number of diseases.

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Inhibition of Both Cyclooxygenase-1 and -2 Promotes Epicutaneous Th2 and Th17 Sensitization and Allergic Airway Inflammation on Subsequent Airway Exposure to Protease Allergen in Mice

International Archives of Allergy and Immunology ◽

10.1159/000514975 ◽

2021 ◽

pp. 1-12

Author(s):

Punyada Suchiva ◽

Toshiro Takai ◽

Seiji Kamijo ◽

Natsuko Maruyama ◽

Takehiko Yokomizo ◽

...

Keyword(s):

Airway Inflammation ◽

Cytokine Production ◽

Allergic Airway Inflammation ◽

Allergic Diseases ◽

Specific Ige ◽

House Dust Mites ◽

Cyclooxygenase 1 ◽

Cox Inhibitor ◽

Allergen Sources ◽

Th17 Cytokine

Introduction: Epicutaneous (e.c.) allergen exposure is an important route of sensitization toward allergic diseases in the atopic march. Allergen sources such as house dust mites contain proteases that involve in the pathogenesis of allergy. Prostanoids produced via pathways downstream of cyclooxygenases (COXs) regulate immune responses. Here, we demonstrate effects of COX inhibition with nonsteroidal anti-inflammatory drugs (NSAIDs) on e.c. sensitization to protease allergen and subsequent airway inflammation in mice. Methods: Mice were treated with NSAIDs during e.c. sensitization to a model protease allergen, papain, and/or subsequent intranasal challenge with low-dose papain. Serum antibodies, cytokine production in antigen-restimulated skin or bronchial draining lymph node (DLN) cells, and airway inflammation were analyzed. Results: In e.c. sensitization, treatment with a nonspecific COX inhibitor, indomethacin, promoted serum total and papain-specific IgE response and Th2 and Th17 cytokine production in skin DLN cells. After intranasal challenge, treatment with indomethacin promoted allergic airway inflammation and Th2 and Th17 cytokine production in bronchial DLN cells, which depended modestly or largely on COX inhibition during e.c. sensitization or intranasal challenge, respectively. Co-treatment with COX-1-selective and COX-2-selective inhibitors promoted the skin and bronchial DLN cell Th cytokine responses and airway inflammation more efficiently than treatment with either selective inhibitor. Conclusion: The results suggest that the overall effects of COX downstream prostanoids are suppressive for development and expansion of not only Th2 but also, unexpectedly, Th17 upon exposure to protease allergens via skin or airways and allergic airway inflammation.

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The Fermented Soy Product ImmuBalanceTM Suppresses Airway Inflammation in a Murine Model of Asthma

Nutrients ◽

10.3390/nu13103380 ◽

2021 ◽

Vol 13 (10) ◽

pp. 3380

Author(s):

Hideaki Kadotani ◽

Kazuhisa Asai ◽

Atsushi Miyamoto ◽

Kohei Iwasaki ◽

Takahiro Kawai ◽

...

Keyword(s):

Bronchoalveolar Lavage ◽

Airway Inflammation ◽

Murine Model ◽

Bronchoalveolar Lavage Fluid ◽

Inflammatory Cell ◽

Allergic Airway Inflammation ◽

Lavage Fluid ◽

Cell Infiltration ◽

Mucus Production ◽

Cell Counts

The fermented soy product ImmuBalance contains many active ingredients and its beneficial effects on some allergic diseases have been reported. We hypothesized that ImmuBalance could have potential effects on airway inflammation in a murine model of asthma. Mice sensitized and challenged with ovalbumin developed airway inflammation. Bronchoalveolar lavage fluid was assessed for inflammatory cell counts and levels of cytokines. Lung tissues were examined for cell infiltration and mucus hypersecretion. Oral administration of ImmuBalance significantly inhibited ovalbumin-induced eosinophilic inflammation and decreased Th2 cytokine levels in bronchoalveolar lavage fluid (p < 0.05). In addition, lung histological analysis showed that ImmuBalance inhibited inflammatory cell infiltration and airway mucus production. Our findings suggest that supplementation with ImmuBalance may provide a novel strategy for the prevention or treatment of allergic airway inflammation.

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Biodegradable antigen-associated PLG nanoparticles tolerize Th2-mediated allergic airway inflammation pre- and postsensitization

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1505782113 ◽

2016 ◽

Vol 113 (18) ◽

pp. 5059-5064 ◽

Cited By ~ 41

Author(s):

Charles B. Smarr ◽

Woon Teck Yap ◽

Tobias P. Neef ◽

Ryan M. Pearson ◽

Zoe N. Hunter ◽

...

Keyword(s):

Airway Inflammation ◽

Significant Risk ◽

Allergic Airway Inflammation ◽

Allergic Diseases ◽

Soluble Antigen ◽

Ag Nps ◽

Th2 Responses ◽

Allergy Treatment ◽

Biodegradable Poly ◽

Induction Of Tolerance

Specific immunotherapy (SIT) is the most widely used treatment for allergic diseases that directly targets the T helper 2 (Th2) bias underlying allergy. However, the most widespread clinical applications of SIT require a long period of dose escalation with soluble antigen (Ag) and carry a significant risk of adverse reactions, particularly in highly sensitized patients who stand to benefit most from a curative treatment. Thus, the development of safer, more efficient methods to induce Ag-specific immune tolerance is critical to advancing allergy treatment. We hypothesized that antigen-associated nanoparticles (Ag-NPs), which we have used to prevent and treat Th1/Th17-mediated autoimmune disease, would also be effective for the induction of tolerance in a murine model of Th2-mediated ovalbumin/alum-induced allergic airway inflammation. We demonstrate here that antigen-conjugated polystyrene (Ag-PS) NPs, although effective for the prophylactic induction of tolerance, induce anaphylaxis in presensitized mice. Antigen-conjugated NPs made of biodegradable poly(lactide-co-glycolide) (Ag-PLG) are similarly effective prophylactically, are well tolerated by sensitized animals, but only partially inhibit Th2 responses when administered therapeutically. PLG NPs containing encapsulated antigen [PLG(Ag)], however, were well tolerated and effectively inhibited Th2 responses and airway inflammation both prophylactically and therapeutically. Thus, we illustrate progression toward PLG(Ag) as a biodegradable Ag carrier platform for the safe and effective inhibition of allergic airway inflammation without the need for nonspecific immunosuppression in animals with established Th2 sensitization.

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Antagonism of mmu-mir-106a attenuates asthma features in allergic murine model

Journal of Applied Physiology ◽

10.1152/japplphysiol.00001.2012 ◽

2012 ◽

Vol 113 (3) ◽

pp. 459-464 ◽

Cited By ~ 68

Author(s):

Amit Sharma ◽

Manish Kumar ◽

Tanveer Ahmad ◽

Ulaganathan Mabalirajan ◽

Jyotirmoi Aich ◽

...

Keyword(s):

Airway Inflammation ◽

Inflammatory Diseases ◽

Allergic Airway Inflammation ◽

Interleukin 10 ◽

Dependent Manner ◽

Th2 Response ◽

Lung Histology ◽

Health And Disease

MicroRNAs (miRs) regulate immunological pathways in health and disease, and a number of miRs have been shown to be altered in mouse models of asthma. The secretion of interleukin-10 (IL-10), an anti-inflammatory cytokine, has been shown to be defective in many inflammatory diseases including asthma. We recently demonstrated that miR-106a inhibits IL-10 in a post-transcriptional manner. In this study, we investigated the effect of inhibition of mmu-miR106a in asthmatic condition to find its possible role as a therapeutic target. Our in vitro experiments with mouse macrophage, RAW264.7, revealed that mmu-miR-106a potentially decreased IL-10 along with increase in proinflammatory cytokine. Furthermore, administration of mmu-miR-106a to naive mice reduced IL-10 levels in lungs in a dose-dependent manner without altering lung histology. Most interestingly, knockdown of mmu-miR-106a in an established allergic airway inflammation has significantly alleviated most of the features of asthma such as airway hyperresponsiveness, airway inflammation, increased Th2 response, goblet cell metaplasia, and subepithelial fibrosis along with increase in IL-10 levels in lung. This represents the first in vivo proof of a miRNA-mediated regulation of IL-10 with a potential to reverse an established asthmatic condition.

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