Experimental diabetes attenuates calcium mobilization and proliferative response in splenic lymphocytes from mice

Satoh, Eiki; Iwasaki, Ryota

doi:10.1007/s12576-010-0117-8

Cited by 4 publications

(2 citation statements)

References 50 publications

(58 reference statements)

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“…It is noteworthy that diabetic animals show marked thymocyte depletion [ 33 ] in association with a reduction in the number of lymphocytes in the peripheral blood [ 34 ]. This lymphopenia observed in diabetics may be due to the occurrence of high levels of apoptosis [ 35 ] and less proliferation of lymphocytes [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Diabetes Downregulates Allergen-Induced Airway Inflammation in Mice

Carvalho

Barreto

Arantes

et al. 2018

Mediators of Inflammation

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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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Section: Discussionmentioning

confidence: 99%

Diabetes Downregulates Allergen-Induced Airway Inflammation in Mice

Carvalho

Barreto

Arantes

et al. 2018

Mediators of Inflammation

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“…Only diabetic mice demonstrated a signi icant reduction in mononuclear cells. Evidence suggests that there is marked a reduction in peripheral lymphocytes because of thymocyte depletion, increased apoptosis and decreased proliferation in diabetes conditions (Barreto et al, 2005;Jung et al, 1999;Otton et al, 2004;Satoh and Iwasaki, 2011).…”

Section: Discussionmentioning

confidence: 99%

Role of Dexamethasone on immune dysregulation mediated through Th1/Th2 cytokine balance in mice challenged with type 1 diabetes and allergic asthma

Ravikumar

2019

ijrps

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Dysregulated equilibrium between T helper 1 (Th1) and T helper 2 (Th2) immune responses has been implicated in the pathogenesis of type 1 diabetes (T1D) and asthma. Conflicting evidence exist explaining the association between T1D and asthma and is still a point of debate. In the present study, our objective was to investigate the influence of associated T1Dco morbid condition on the induction of experimental asthma in mice and also to evaluate the efficacy of Dexamethasone (0.5 mg/kg, s.c.ly) in these mice. Type 1 diabetes was induced by a single intravenous injection of alloxan (80 mg/kg) in Balb/c mice. Following diabetes induction, mice were sensitized with an intraperitoneal injection of 50 µg ovalbumin (Ova) emulsified in 2.5 mg aluminum hydroxide on days 3 and 8. From day 13 to day 15, animals were challenged intranasally with 100 µg Ova in 25 µl of sterile saline. Dexamethasone treatment was initiated on sensitization day and continued once in 2 days thereafter until day 15. Control animals received only saline without Ova. On day 16, mice were subjected to nasal hyperresponsiveness (NHR) immediately after the Ova challenge. Bronchioalveolar lavage fluid (BALF), blood, and lungs were collected 1h post completion of NHR for further analysis. Alloxan diabetic mice showed significantly lower levels of eosinophils in BALF and blood with the corresponding decrease in inflammatory cells around airways in hematoxylin & eosin-stained lung sections, but with no change in NHR than in non-diabetics after Ova sensitization and challenge. Dexamethasone treatment showed a significant reduction of airway inflammation and related Th2 immune responses, with a lesser magnitude of efficacy in diabetic asthma mice than in non-diabetic asthma mice. The presence of T1D featured a unique, yet the intermediary stage of asthma induction and also presented an altered magnitude of Dexamethasone efficacy compared to the absence of T1D in the murine model of Ova induced asthma.

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