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The fish gills represent a crucial organ for the communication with the aquatic environment. Transcriptional changes in gills of two hatchery rainbow trout strains in response to injection with the potent pathogen Aeromonas salmonicida were detected by global gene expression profiling using a 4×44K oligonucleotide microarray. Emphasis was placed on "day 3 postinfection" representing a decisive time point for the resolution of inflammation. The comparison of features and pathways differentially regulated in branchial tissues revealed that the local breeding strain BORN and imported American rainbow trout apply common and specific immune strategies. In gills of infected BORN trout, we observed a dynamic regulation of genes controlling NF-κB pathways and the induction of factors promoting the development of myeloid cells, whereas an increased expression of lysozyme and immunoglobulin genes was obvious in gills of infected import trout. In order to prove the relevance of the array-predicted candidates as well as well-known immune genes for gill immunity, a subsequent in vitro experiment was conducted. Altogether, we uncovered dynamic but moderate changes in the expression of a broad range of immune-relevant features implying the gill's involvement in pathogen defense strategies.

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Atopic dermatitis (AD) is an inflammatory dermatosis with a pathogenesis believed to be due to a combination of genetic, immunologic and environmental factors that affects up to 5% of adults and 20% of children worldwide. 1,2 Common genetic factors include polymorphisms in the filaggrin structural protein, interleukin (IL)-4 receptor and vitamin D receptor. [3][4][5] AD is driven by multiple immune pathways, most commonly with activation of Th2 and Th22 T-cell subsets. 6 Crosstalk between commensals and the host immune system modulates adaptive and innate immune responses in AD. 7 Staphylococcus aureus (SA) in AD lesions and surrounding normal skin was first noted by Leyden et al. in the 1970s; since then, the understanding of its role in AD has drastically evolved. 8,9 SA is a well-established exacerbator of AD; it is frequently isolated from the skin of AD patients and increased SA density is found during flares. 10 A meta-analysis in 2016 reported a pooled prevalence of SA colonization among AD patients of 70% in lesional skin, 39% in non-lesional skin and 62% in the nose. 11 More recently, Kong et al 12 found that AD treatments and flares were closely associated with shifts in the cutaneous microbial diversity. While current evidence has established that SA proliferates during flares and plays a role in the cycle of epidermal breakdown and inflammation, a true causal relationship has not been established. Herein, we will summarize the

Neurologic symptoms secondary to a paraneoplastic syndrome may be the presenting manifestation of a previously undiagnosed cancer, and alertness to these syndromes may provide an opportunity for early detection and treatment of a cancer. Paraneoplastic weakness is a rare manifestation of renal cell carcinoma and may present with variable electrophysiological features. We present a case of a patient with progressive weakness, sensory changes, and urinary retention, with electrophysiological features suggestive of a complex peripheral nervous system syndrome. Ultimately, a renal cell mass was detected and resected, resulting in significant clinical improvement. We review the literature, cataloging the known neurologic syndromes and antibodies associated with renal cell carcinoma. This case highlights that paraneoplastic neurological disorders associated with RCC can take on many features and provides a resource to practitioners for early detection of a neurologic paraneoplastic syndrome arising from renal cell carcinoma.