Mucosal Immunity

A century after they were discovered killing diarrhea-causing bacteria in the feces of World War I soldiers, the viruses known as bacteriophages, or simply phages, are drawing new attention for the role they might play within the human body. Phages have been found most everywhere, from oceans to soils. Now, a study suggests that people absorb up to 30 billion phages every day through their intestines. Though where those viruses end up is unclear, those data and other recent studies have some scientists wondering whether a sea of phages within the human body—a "phageome"—might play a key role in our physiology, perhaps by regulating our immune system.

Tuberculosis (TB) causes more annual deaths globally than any other infectious disease. However, progress in developing novel vaccines, diagnostics and therapies has been hampered by an incomplete understanding of the immune response to Mycobacterium tuberculosis (Mtb). While the role of many immune cells has been extensively explored, mast cells (MCs) have been relatively ignored. MCs are tissue resident cells involved in defense against bacterial infections playing an important role mediating immune cell crosstalk. This review discusses specific interactions between MCs and Mtb, their contribution to both immunity and disease pathogenesis and explores their role in orchestrating other immune cells against infections.

Letter

In recent years, various technological developments markedly improved imaging of mucosal inflammation in patients with inflammatory bowel diseases. Whereas technological developments such as high-definition-, chromo- and autofluorescence-endoscopy led to a more precise and detailed assessment of mucosal inflammation during wide-field endoscopy, probe-based and stationary confocal laser microscopy enabled in vivo real-time microscopic imaging of mucosal surfaces within the gastrointestinal tract. Through the use of fluorochromes with specificity against a defined molecular target combined with endoscopic techniques that allow ultrastructural resolution, molecular imaging enables in vivo visualization of single molecules or receptors during endoscopy. Molecular imaging has therefore greatly expanded the clinical utility and applications of modern innovative endoscopy, now including not only diagnosis, surveillance, and treatment but also the prediction of individual therapeutic response. Furthermore, non-invasive imaging techniques such as computed tomography, magnetic resonance imaging, scintigraphy and ultrasound provide helpful information as supplement to invasive endoscopic procedures. In this review, we provide an overview on the current status of advanced imaging technologies for the clinical non-invasive and endoscopic evaluation of mucosal inflammation. Furthermore, the value of novel methods such as multiphoton microscopy, optoacoustics and optical coherence tomography and their possible future implementation into clinical diagnosis and evaluation of mucosal inflammation will be discussed.

Alveolar macrophage (AM) development depends on GM-CSF, but whether additional factors
regulate AMs is unknown. Yu et al. identified TGF-β as another cytokine critical for
the development and maturation of AMs. TGF-β regulated AMs in an autocrine manner
and was also essential for their self-maintenance in adult mice.

Characterization of a wild mice reference microbiome opens a window of opportunity
to understand how the gut microbiota affects aspects of host physiology that are important
in the natural world outside the laboratory.

Primer

Immune responses to fungal infections are complicated by the fact that fungi can exist in multiple forms depending on environmental cues. Here, Verma et al . have evaluated innate immune responses to Candida albicans , a fungus that transitions from yeast to filamentous hyphae as infection progresses. They find that candidalysin, a hypha-associated protein and virulence factor, serves as a danger signal that potentiates the immune response to C. albicans . Candidalysin-deficient strains of C. albicans caused minimal epithelial damage and elicited a blunted type 17 immune response. The authors propose that the innate antifungal responses to C. albicans are driven by a synergy between cellular damage triggered by candidalysin that is further amplified by interleukin-17 driven inflammation.

Review