Innate lymphoid cells at the interface between obesity and asthma

Abstract

SummaryObesity and asthma prevalence has dramatically and concomitantly increased over the last 25 years, and many epidemiological studies have highlighted obesity as an important risk factor for asthma. Although many studies have been performed, the underlying mechanisms remain poorly understood. Innate mechanisms have been involved in both diseases, in particular through the recently described innate lymphoid cells (ILCs). ILCs are subdivided into three groups that are defined by their cytokine production and by their master transcription factor expression, in sharp correlation with their T helper counterparts. However, unlike T helper cells, ILCs do not express antigen-specific receptors, but respond to damage-induced signals. ILCs have been found in target tissues of both diseases, and data have implicated these cells in the pathogenesis of both diseases. In particular group 2 ILCs (ILC2) are activated in both the adipose and lung tissues under the effect of interleukin-33 and interleukin-25 expression. However, counter-intuitively to the well-known association between obesity and asthma, ILC2 are beneficial for obesity but deleterious for asthma. This review will examine the roles of ILCs in each disease and recent data highlighting ILCs as a putative link between obesity and asthma.

Maternal high fat diet compromises survival and modulates lung development of offspring, and impairs lung function of dams (female mice)

“…Similarly, we also observed reduced levels of the innate Th2 cell-promoting cytokine IL-33, and the adipokine, leptin in the lungs of dams fed a high fat diet that were pregnant twice. Interestingly, increased expression of these mediators has been shown to promote asthma exacerbation and airway hyper-reactivity in animal models [47]. Furthermore, reduced tissue elastance (and adiponectin levels in BALF) was observed in the offspring of the second pregnancy of dams fed either diet; suggesting that there may be protective effects of a second pregnancy that extend to the offspring in some developmental niches (i.e.…”

Tertiary lymphoid structure related B-cell IgE isotype switching and secondary lymphoid organ linked IgE production in mouse allergy model

“…Very often, although not always, the level of leptin in patients with obesity is increased, and the level of adiponectin is reduced [ 7 , 8 ]. It was shown that the administration of leptin to BALB/c mice increased the intensity of allergic inflammation and production of IgE while the administration of adiponectin inhibited it [ 8 – 10 ]. It is especially important to note that adipose tissue contains TLSs, although their number varies depending on the anatomical location [ 11 ].…”

Adipokines and the control of mast cell functions: from obesity to inflammation?

“…The chronic inflammation that results from high levels of adiposity is associated with the development of a number of inflammatory conditions, mediated in part through profound effects of adipokines on a broad range of immune cells, including dendritic cells, innate lymphoid cells, and neutrophils . This new understanding of how mast cells respond to leptin and adiponectin adds another piece to this puzzle.…”