scholarly journals The immune response of inbred laboratory mice to Litomosoides sigmodontis : A route to discovery in myeloid cell biology

2020 ◽  
Vol 42 (7) ◽  
Author(s):  
Conor M. Finlay ◽  
Judith E. Allen
2018 ◽  
Vol 56 (1) ◽  
pp. 513-533 ◽  
Author(s):  
Jiejie Li ◽  
Christopher J. Staiger

The plant cytoskeleton is a dynamic framework of cytoplasmic filaments that rearranges as the needs of the cell change during growth and development. Incessant turnover mechanisms allow these networks to be rapidly redeployed in defense of host cytoplasm against microbial invaders. Both chemical and mechanical stimuli are recognized as danger signals to the plant, and these are perceived and transduced into cytoskeletal dynamics and architecture changes through a collection of well-recognized, previously characterized players. Recent advances in quantitative cell biology approaches, along with the powerful molecular genetics techniques associated with Arabidopsis, have uncovered two actin-binding proteins as key intermediaries in the immune response to phytopathogens and defense signaling. Certain bacterial phytopathogens have adapted to the cytoskeletal-based defense mechanism during the basal immune response and have evolved effector proteins that target actin filaments and microtubules to subvert transcriptional reprogramming, secretion of defense-related proteins, and cell wall–based defenses. In this review, we describe current knowledge about host cytoskeletal dynamics operating at the crossroads of the molecular and cellular arms race between microbes and plants.


2016 ◽  
Vol 27 (3) ◽  
pp. 483-490 ◽  
Author(s):  
Shengyi Sun ◽  
Rohan Lourie ◽  
Sara B. Cohen ◽  
Yewei Ji ◽  
Julia K. Goodrich ◽  
...  

Inflammatory bowel disease (IBD) is an incurable chronic idiopathic disease that drastically decreases quality of life. Endoplasmic reticulum (ER)–associated degradation (ERAD) is responsible for the clearance of misfolded proteins; however, its role in disease pathogenesis remains largely unexplored. Here we show that the expression of SEL1L and HRD1, the most conserved branch of mammalian ERAD, is significantly reduced in ileal Crohn’s disease (CD). Consistent with this observation, laboratory mice with enterocyte-specific Sel1L deficiency (Sel1LΔIEC) develop spontaneous enteritis and have increased susceptibility to Toxoplasma gondii–induced ileitis. This is associated with profound defects in Paneth cells and a disproportionate increase of Ruminococcus gnavus, a mucolytic bacterium with known association with CD. Surprisingly, whereas both ER stress sensor IRE1α and effector CHOP are activated in the small intestine of Sel1LΔIEC mice, they are not solely responsible for ERAD deficiency–associated lesions seen in the small intestine. Thus our study points to a constitutive role of Sel1L-Hrd1 ERAD in epithelial cell biology and the pathogenesis of intestinal inflammation in CD.


2006 ◽  
Vol 43 (4) ◽  
pp. 203-207 ◽  
Author(s):  
A. Perec ◽  
A. Okulewicz

AbstractIn conventional mice colonies, mouse pinworm, Syphacia obvelata is found very often. Several studies indicate that infection with this parasite can modulate the immune system of the host and can affect experimental final results. The aim of our study was to investigate the most immunogenic proteins of S. obvelata inducing both local and systemic immune response in naturally infected laboratory mice. Protein extracts of S. obvelata were analysed by Western blotting to examine their antigenic character. The antigens were probed with serum and mucosa of S. obvelata naturally infected mice. Surface and somatic antigens were recognized by serum and mucosal IgG, IgA and IgM antibodies. The most immunogenic and dominant proteins were observed. Proteins of Mw ∼ 70, 65 and 48 kDa showed the most evident reaction with serum and mucosa antibodies of infected animals. Surface and somatic antigens of nematode S. obvelata eliciting immune response in laboratory mice may be useful in development of a diagnostic test which could be applied for the infection control prior the experiments.


Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. SCI-45-SCI-45
Author(s):  
Mukesh Jain

Abstract Armed with the appreciation that the blood and vascular system share common origins and cooperate to ensure fundamental processes (e.g. blood flow/fluidity, oxygen/nutrient delivery, immunity) essential for organismal survival, we posited that shared molecular pathways may be operative in coordinating the function of both systems. Over the past 2 decades, studies from our group and others have identified a family of transcription factors termed Kruppel-like factors (KLFs) as essential for development, differentiation, and function of cellular constituents of both the hematopoietic and vascular systems. In this presentation, discussion will focus on the role KLFs in control of endothelium and myeloid cell biology in physiology and disease. Specifically, cellular and in vivo evidence will be discussed implicating KLFs as master regulators of all cardinal endothelial functions (permeability, vasoreactivity, blood fluidity, and inflammation). Further, studies demonstrating KLF-control of myeloid cell development, subset specification, and pro-inflammatory activation will be reviewed with particular emphasis on results of efforts altering myeloid KLFs in the context of acute (e.g. bacterial infection, sepsis) and chronic (e.g. atherosclerosis, arterial/venous thrombosis) inflammatory processes. Correlative studies in human subjects will be presented. And finally, insights into how targeting KLFs can be exploited for therapeutic gain will be discussed. Disclosures No relevant conflicts of interest to declare.


F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 1647 ◽  
Author(s):  
Andrea Reboldi ◽  
Eric Dang

It has been long recognized that cholesterol is a critical molecule in mammalian cell biology, primarily for its contribution to the plasma membrane’s composition and its role in assuring proper transmembrane receptor signaling as part of lipid rafts. Efforts have also been made to characterize the cholesterol biosynthetic pathway, cholesterol homeostasis, and cholesterol-derived metabolites in order to gain insights into their dysregulation during metabolic diseases. Despite the central role cholesterol metabolism plays in shaping human health, its regulation during immune activation, such as immune response to pathogens or autoimmune/autoinflammatory diseases, is poorly understood. The immune system is composed of several type of cells with distinct developmental origin, life span, molecular requirements, and gene expressions. It is unclear whether the same array of cholesterol metabolism regulators are equally employed by different immune cells and whether distinct cholesterol metabolites have similar biological consequences in different immune cells. In this review, we will describe how cholesterol metabolism is controlled during the adaptive and the innate immune response and the role for intracellular and extracellular receptors for cholesterol and its derivatives.


2000 ◽  
Vol 113 (19) ◽  
pp. 3355-3356
Author(s):  
P.J. Sansonetti

Advances in Cell and Molecular Biology of Membranes and Organelles Volume 5 - Phagocytosis: the Host edited by Alan M. Tartakoff; volume editor, Siamon Gordon JAI Press Inc./Ablex Publishing Corp. (1999) pp. 521. ISBN 1–55938-999-0 $147.50 Over the last few years, cell biology has become a dominant approach in several disciplines of the life sciences, including the study of phagocytic cells! Before, with exceptions, the science of phagocytosis had often remained descriptive, with microbiologists providing detailed descriptions of the various types and stages of internalization and killing or survival of the pathogenic microorganisms, and immunologists providing an exhaustive description of the complex processes of microbe degradation, antigen processing and presentation following the phagocytic process per se. Phagocytosis: the Host excellently reflects the revolution that has occurred in this field. In other words, the science of phagocytosis is now dominated by an analytical approach based on deciphering the signals that carry out each of the critical steps of the process. Edited by a master of the discipline, in 21 chapters, this book - with great justice dedicated to the late Zanvil A. Cohn - covers the molecular and cellular aspects of phagocytic processes in a logical progression. The best specialists in the field have risen to the challenge. Four chapters are devoted to receptors, certainly representing one of the best and most exhaustive current reviews of this field. Of particular interest are the recent developments on scavenging receptors with regard to phagocytosis of both microbes and apoptotic bodies. In the next three chapters, signalling makes a spectacular entry: our knowledge of the molecular mechanisms that regulate the cytoskeleton is exponentially increasing and finds here its perfect niche. To this section might have been added the chapter entitled ‘The Phagocytic Actin Cytoskeleton’, which appears in the next section of four chapters devoted to ‘the pathway’, in other words, the maturation of phagosomes. Here again, progress has been tremendous in understanding the logics of maturation pathways and we are very much looking forward to the next volume Phagocytosis: the Microbes, which will show how these microbes can perturb, to their profit, phagosomal maturation in order to ‘carve’ a niche which permits their survival. A splendid example of coevolution. The last five chapters form a section (Responses) that encompasses most of the effector mechanisms that link the phagocytic event to the immune response, a domain that dictates the subtle transition between the innate and the adaptative immune response. The antimicrobial mechanisms of phagocytic cells are largely described here, including antimicrobial peptides, in often overlapping chapters. This does not matter at all because, again, the best specialists have gathered to produce a single chapter and the science presented is of the highest quality. So, altogether, this is a splendid contribution that will represent a keystone in the fast moving field of phagocytosis. If this reader had one criticism, it would be the illustrations. For a field that is extremely prone to rich illustrations, figures are generally scarce and grey, and the reproduction of the electron microscopy images is generally poor in definition, brightness and contrast. This should not deter anyone interested in the field from acquiring this volume and its brother volume on interactions with microbes. No doubt this, for the years to come, will be a reference text for phagocytosis. Microbiologists, immunologists and cell biologists, both students and senior scientists will find here updated information and all the relevant and most recent references (up to 2500).


2021 ◽  
Vol 12 ◽  
Author(s):  
Jingming Zhuang ◽  
Jiangang Hou

Kidney transplantation is a primary therapy for end-stage renal disease (ESRD) all the time. But it does not mean that we have fully unraveling the mystery of kidney transplantation and confer every patient favorable prognosis. Immune rejection has always been a stumbling block when we try to increase the success rate of kidney transplantation and improve long-term outcomes. Even if the immune rejection is effectively controlled in acute phase, there is a high possibility that the immune response mediated by chronically activated antibodies will trigger chronic rejection and ultimately lead to graft failure. At present, immunosuppressive agent prepared chemically is mainly used to prevent acute or chronic rejection, but it failed to increase the long-term survival rate of allografts or reduce the incidence of chronic rejection after acute rejection, and is accompanied by many adverse reactions. Therefore, many studies have begun to use immune cells to regulate the immune response in order to control allograft rejection. This article will focus on the latest study and prospects of more popular regulatory myeloid cells in the direction of renal transplantation immunotherapy and introduce their respective progress from experimental research to clinical research.


2021 ◽  
Vol 6 ◽  
pp. 68
Author(s):  
Zoe Lee Hore ◽  
Sara Villa-Hernandez ◽  
Franziska Denk

Background: Chemotherapy-induced peripheral neuropathy (CIPN) is a disabling side effect of various chemotherapeutic agents, including oxaliplatin. It is highly prevalent amongst cancer patients, causing sensory abnormalities and pain. Unfortunately, as the underlying mechanisms remain poorly understood, effective therapeutics are lacking. Neuro-immune interactions have been highlighted as potential contributors to the development and maintenance of CIPN, however, whether this is the case in oxaliplatin-induced peripheral neuropathy (OIPN) is yet to be fully established. Methods: In this study we used flow cytometry to examine the peripheral immune response of male C57BL/6 mice following both single and repeated oxaliplatin administration. In animals exposed to repeated dosing, we also undertook mechanical and thermal behavioural assays to investigate how oxaliplatin alters phenotype, and conducted RT-qPCR experiments on bone marrow derived macrophages in order to further inspect the effects of oxaliplatin on immune cells. Results: In contrast to other reports, we failed to observe substantial changes in overall leukocyte, lymphocyte or myeloid cell numbers in dorsal root ganglia, sciatic nerves or inguinal lymph nodes. We did however note subtle, tissue-dependant alterations in several myeloid subpopulations following repeated dosing. These included a significant reduction in MHCII antigen presenting cells in the sciatic nerve and an increase in infiltrating cell types into the inguinal lymph nodes. Though repeated oxaliplatin administration had a systemic effect, we were unable to detect a pain-like behavioural phenotype in response to either cold or mechanical stimuli. Consequently, we cannot comment on whether the observed myeloid changes are associated with OIPN. Conclusions: Our discussion puts these results into the wider context of the field, advocating for greater transparency in reporting, alignment in experimental design and the introduction of more clinically relevant models. Only through joint concerted effort can we hope to increase our understanding of the underlying mechanisms of CIPN, including any immune contributions.


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