Surgical and physical stress increases circulating blood dendritic cell counts independently of monocyte counts

Blood ◽  
2001 ◽  
Vol 98 (1) ◽  
pp. 140-145 ◽  
Author(s):  
Christopher S. K. Ho ◽  
Jose Alejandro López ◽  
Slavica Vuckovic ◽  
Christopher M. Pyke ◽  
Richard L. Hockey ◽  
...  
Keyword(s):  
The Body ◽  
Exercise Stress ◽  
Primary Immune Response ◽  
Cell Counts ◽  
Elective Laparoscopic Cholecystectomy ◽  
And Function ◽  
Antigen Presenting ◽  
Blood Dendritic Cell ◽  
Unique Ability

Dendritic cells (DCs) are specialized antigen-presenting cells that have the unique ability to initiate a primary immune response. The effect of physiologic stress on circulating blood DCs has thus far not been studied. In this study, we applied a recently developed method of counting blood DCs to test the hypothesis that significant stress to the body such as surgery and exercise might induce measurable changes in the DC numbers, subsets, phenotype, and function. Twenty-six patients scheduled for elective laparoscopic cholecystectomy, 4 for elective hysterectomy, 56 controls, and 5 volunteers who underwent a stress exercise test were enrolled in the study. Absolute DC counts increased acutely (71.7% ± 11% [SEM],P = .0001) in response to the stress of surgery and dropped below preoperative levels (−25% ± 14% [SEM],P = .05) on days 2-3. The perioperative DC subset balance remained constant. Interestingly, DC counts changed independently of monocyte counts. Exercise also induced a rise in DC counts but coincidentally with monocyte counts. Surprisingly, no phenotypic or functional activation of DCs was seen in either stress situations in vivo. DCs are rapidly mobilized into the circulation in response to surgical and exercise stress, which may serve to prepare the host's immune defenses against trauma. The independent regulation of the DC and monocyte counts reinforces the distinction between these 2 cell populations.

Surgical and physical stress increases circulating blood dendritic cell counts independently of monocyte counts

Blood ◽  
2001 ◽  
Vol 98 (1) ◽  
pp. 140-145 ◽  
Author(s):  
Christopher S. K. Ho ◽  
Jose Alejandro López ◽  
Slavica Vuckovic ◽  
Christopher M. Pyke ◽  
Richard L. Hockey ◽  
...  
Keyword(s):  
The Body ◽  
Exercise Stress ◽  
Primary Immune Response ◽  
Cell Counts ◽  
Elective Laparoscopic Cholecystectomy ◽  
And Function ◽  
Antigen Presenting ◽  
Blood Dendritic Cell ◽  
Unique Ability

Abstract Dendritic cells (DCs) are specialized antigen-presenting cells that have the unique ability to initiate a primary immune response. The effect of physiologic stress on circulating blood DCs has thus far not been studied. In this study, we applied a recently developed method of counting blood DCs to test the hypothesis that significant stress to the body such as surgery and exercise might induce measurable changes in the DC numbers, subsets, phenotype, and function. Twenty-six patients scheduled for elective laparoscopic cholecystectomy, 4 for elective hysterectomy, 56 controls, and 5 volunteers who underwent a stress exercise test were enrolled in the study. Absolute DC counts increased acutely (71.7% ± 11% [SEM],P = .0001) in response to the stress of surgery and dropped below preoperative levels (−25% ± 14% [SEM],P = .05) on days 2-3. The perioperative DC subset balance remained constant. Interestingly, DC counts changed independently of monocyte counts. Exercise also induced a rise in DC counts but coincidentally with monocyte counts. Surprisingly, no phenotypic or functional activation of DCs was seen in either stress situations in vivo. DCs are rapidly mobilized into the circulation in response to surgical and exercise stress, which may serve to prepare the host's immune defenses against trauma. The independent regulation of the DC and monocyte counts reinforces the distinction between these 2 cell populations.

scholarly journals Physiological and Disease Models of Respiratory System Based on Organ-on-a-Chip Technology

Micromachines ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 1106
Author(s):  
Di Wang ◽  
Ye Cong ◽  
Quanfeng Deng ◽  
Xiahe Han ◽  
Suonan Zhang ◽  
...  
Keyword(s):  
Respiratory Diseases ◽  
Solute Concentration ◽  
The Body ◽  
The Real ◽  
Growth State ◽  
Chip Technology ◽  
Organ On A Chip ◽  
And Function ◽  
Multiple Cells

The pathogenesis of respiratory diseases is complex, and its occurrence and development also involve a series of pathological processes. The present research methods are have difficulty simulating the natural developing state of the disease in the body, and the results cannot reflect the real growth state and function in vivo. The development of microfluidic chip technology provides a technical platform for better research on respiratory diseases. The size of its microchannel can be similar to the space for cell growth in vivo. In addition, organ-on-a-chip can achieve long-term co-cultivation of multiple cells and produce precisely controllable fluid shear force, periodically changing mechanical force, and perfusate with varying solute concentration gradient. To sum up, the chip can be used to analyze the specific pathophysiological changes of organs meticulously, and it is widely used in scientific research on respiratory diseases. The focus of this review is to describe and discuss current studies of artificial respiratory systems based on organ-on-a-chip technology and to summarize their applications in the real world.

scholarly journals Activated Complement Component 3 (C3) Is Required for Ultraviolet Induction of Immunosuppression and Antigenic Tolerance

1998 ◽  
Vol 187 (7) ◽  
pp. 1133-1138 ◽  
Author(s):  
Craig Hammerberg ◽  
Santosh K. Katiyar ◽  
Michael C. Carroll ◽  
Kevin D. Cooper
Keyword(s):  
Normal Skin ◽  
Complement Component ◽  
Primary Immune Response ◽  
Contact Sensitivity ◽  
Exposed Skin ◽  
Class Ii Mhc ◽  
Primary Sensitization ◽  
Antigen Presenting ◽  
Complement Component 3

Complement component 3 (C3), a critical regulator of innate immunity, may also play a role in the regulation of cognate immunity, such as contact sensitivity responses. Because ultraviolet (UV) radiation also activates C3 in the skin, we determined whether the immunosuppressed state that results when a contact sensitizer is applied through UVB-exposed skin requires the presence and activation of C3. This question was addressed through the use of C3-deficient mice, blockade of C3 cleavage to C3b, and accelerated degradation of iC3b by soluble complement receptor 1 (sCR1). Both C3-modulated systems totally reversed the failure to induce a contact sensitivity response to dinitrofluorobenzene (DNFB) upon primary sensitization at the UV-exposed site, as well as immunologic tolerance to a second DNFB immunization through normal skin. Treatment with sCR1 reduced the infiltration of CD11b+ leukocytes into the epidermis and dermis of UV-irradiated skin but did not reverse the UV-induced depletion of epidermal class II MHC+CD11blo Langerhans cells. These data, taken together with previous results showing abrogation of locally induced UV immunosuppression by in vivo anti-CD11b treatment, suggest a novel mechanism by which ligation of the leukocyte β2 integrin, CD11b, by iC3b molecules formed from C3 activation in UV-exposed skin, modifies cutaneous CD11b+ cells such that skin antigen-presenting cells are unable to sensitize in a primary immune response, but actively induce antigenic tolerance.

scholarly journals Posttranslational Modifications and the Immunogenicity of Biotherapeutics

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Roy Jefferis
Keyword(s):  
Posttranslational Modifications ◽  
Drug Product ◽  
Molecular Forms ◽  
Phagocytic Cells ◽  
Production Platform ◽  
The Individual ◽  
And Function ◽  
Antigen Presenting

Whilst the amino acid sequence of a protein is determined by its gene sequence, the final structure and function are determined by posttranslational modifications (PTMs), including quality control (QC) in the endoplasmic reticulum (ER) and during passage through the Golgi apparatus. These processes are species and cell specific and challenge the biopharmaceutical industry when developing a production platform for the generation of recombinant biologic therapeutics. Proteins and glycoproteins are also subject to chemical modifications (CMs) bothin vivoandin vitro. The individual is naturally tolerant to molecular forms of self-molecules but nonself variants can provoke an immune response with the generation of anti-drug antibodies (ADA); aggregated forms can exhibit enhanced immunogenicity and QC procedures are developed to avoid or remove them. Monoclonal antibody therapeutics (mAbs) are a special case because their purpose is to bind the target, with the formation of immune complexes (ICs), a particular form of aggregate. Such ICs may be removed by phagocytic cells that have antigen presenting capacity. These considerations may frustrate the possibility of ameliorating the immunogenicity of mAbs by rigorous exclusion of aggregates from drug product. Alternate strategies for inducing immunosuppression or tolerance are discussed.

scholarly journals Role of Exosomes in Islet Transplantation

2021 ◽  
Vol 12 ◽  
Author(s):  
Jordan Mattke ◽  
Srividya Vasu ◽  
Carly M. Darden ◽  
Kenjiro Kumano ◽  
Michael C. Lawrence ◽  
...  
Keyword(s):  
Islet Transplantation ◽  
Graft Function ◽  
Pancreatic Islet Transplantation ◽  
Complex Molecules ◽  
Wide Range ◽  
And Function ◽  
Antigen Presenting

Exosomes are known for their ability to transport nucleic acid, lipid, and protein molecules, which allows for communication between cells and tissues. The cargo of the exosomes can have a variety of effects on a wide range of targets to mediate biological function. Pancreatic islet transplantation is a minimally invasive cell replacement therapy to prevent or reverse diabetes mellitus and is currently performed in patients with uncontrolled type 1 diabetes or chronic pancreatitis. Exosomes have become a focus in the field of islet transplantation for the study of diagnostic markers of islet cell viability and function. A growing list of miRNAs identified from exosomes collected during the process of isolating islets can be used as diagnostic biomarkers of islet stress and damage, leading to a better understanding of critical steps of the isolation procedure that can be improved to increase islet yield and quality. Exosomes have also been implicated as a possible contributor to islet graft rejection following transplantation, as they carry donor major histocompatibility complex molecules, which are then processed by recipient antigen-presenting cells and sensed by the recipient immune cells. Exosomes may find their way into the therapeutic realm of islet transplantation, as exosomes isolated from mesenchymal stem cells have shown promising results in early studies that have seen increased viability and functionality of isolated and grafted islets in vitro as well as in vivo. With the study of exosomes still in its infancy, continued research on the role of exosomes in islet transplantation will be paramount to understanding beta cell regeneration and improving long-term graft function.

scholarly journals Skeletal muscle releases extracellular vesicles with distinct protein and miRNA signatures that accumulate and function within the muscle microenvironment

2021 ◽  
Author(s):  
Sho Watanabe ◽  
Yuri Sudo ◽  
Satoshi Kimura ◽  
Kenji Tomita ◽  
Makoto Noguchi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Extracellular Vesicles ◽  
Cell Types ◽  
The Body ◽  
C2c12 Cells ◽  
Ips Cell ◽  
Potential Marker ◽  
And Function ◽  
Intercellular Communications

Extracellular vesicles (EVs) contain various regulatory molecules and mediate intercellular communications. Although EVs are secreted from various cell types, including skeletal muscle cells, and present in the blood, their identity is poorly characterized in vivo, limiting the identification of their origin in the blood. Since the skeletal muscle is the largest organ in the body, it could substantially contribute to circulating EVs as their source. However, due to the lack of defined markers that distinguish SkM-EVs from others, whether the skeletal muscle releases EVs in vivo and how much the skeletal muscle-derived EVs (SkM-EVs) account for plasma EVs remain poorly understood. In this work, we perform quantitative proteomic analyses on EVs released from C2C12 cells and human iPS cell-derived myocytes and identify potential marker proteins that mark SkM-EVs. These markers we identified apply to in vivo tracking of SkM-EVs. The results show that skeletal muscle makes only a subtle contribution to plasma EVs as their source in both control and exercise conditions in mice. On the other hand, we demonstrate that SkM-EVs are concentrated in the skeletal muscle interstitium. Furthermore, we show that interstitium EVs are highly enriched with the muscle-specific miRNAs and repress the expression of the paired box transcription factor Pax7, a master regulator for myogenesis. Taken together, our findings reveal that the skeletal muscle releases exosome-like small EVs with distinct protein and miRNA profiles in vivo and that SkM-EVs mainly play a role within the muscle microenvironment where they accumulate.

Nanofiber Micropatterns for Controlled Release of Biomolecules

2011 ◽  
Author(s):  
Walter Bonani ◽  
Claudio Migliaresi ◽  
Wei Tan
Keyword(s):  
The Body ◽  
Biodegradable Materials ◽  
Signal Molecules ◽  
3 Dimensional ◽  
The Past ◽  
Direct Delivery ◽  
And Function ◽  
Vascular Formation

Essential to growing or regenerating 3-dimensional tissues is the formation of functional microcirculation that provides nutrients, oxygen and signal molecules for tissue survival and function regeneration. In the past decade, molecule-based microvascular formation has been achieved in vitro and in vivo. However, direct delivery of angiogenic molecules often results in malformed hyperpermeable microvessels, microvessels with low density. This can be attributed to the lack of effective molecule mechanisms that regulate vascular formation. More recent studies utilize biodegradable materials to control the delivery of biomolecules for vascularization of engineered or ischemic tissues, and exciting results have shown the importance of molecule kinetics to the vascular formation. Molecule delivery mechanisms that mimic precisely-regulated spatiotemporal signaling events during natural vascularization may be a possible way to improve or optimize the process. Hence, this study is designed to develop a new release system capable of degrading in the body and releasing biomolecules in a spatiotemporally controlled manner.

scholarly journals Chemokine and chemokine receptor expression during colony stimulating factor-1–induced osteoclast differentiation in the toothless osteopetrotic rat: a key role for CCL9 (MIP-1γ) in osteoclastogenesis in vivo and in vitro

Blood ◽  
2006 ◽  
Vol 107 (6) ◽  
pp. 2262-2270 ◽  
Author(s):  
Meiheng Yang ◽  
Geneviève Mailhot ◽  
Carole A. MacKay ◽  
April Mason-Savas ◽  
Justin Aubin ◽  
...  
Keyword(s):  
Osteoclast Differentiation ◽  
The Body ◽  
Receptor Expression ◽  
Long Bone ◽  
Tartrate Resistant Acid Phosphatase ◽  
Colony Stimulating Factor ◽  
Cell Counts ◽  
Stimulating Factor

AbstractOsteoclasts differentiate from hematopoietic precursors under systemic and local controls. Chemokines and receptors direct leukocyte traffic throughout the body and may help regulate site-specific bone resorption. We investigated bone gene expression in vivo during rapid osteoclast differentiation induced by colony-stimulating factor 1 (CSF-1) in Csf1-null toothless (tl/tl) rats. Long-bone RNA from CSF-1–treated tl/tl rats was analyzed by high-density microarray over a time course. TRAP (tartrate-resistant acid phosphatase)–positive osteoclasts appeared on day 2, peaked on day 4, and decreased slightly on day 6, as marrow space was expanding. TRAP and cathepsin K mRNA paralleled the cell counts. We examined all chemokine and receptor mRNAs on the arrays. CCL9 was strongly induced and peaked on day 2, as did its receptor, CCR1, and regulatory receptors c-Fms (CSF-1 receptor) and RANK (receptor activator of nuclear factor κB). Other chemokines and receptors showed little or no significant changes. In situ hybridization and immunohistochemistry revealed CCL9 in small, immature osteoclasts on day 2 and in mature cells at later times. Anti-CCL9 antibody inhibited osteoclast differentiation in culture and significantly suppressed the osteoclast response in CSF-1–treated tl/tl rats. While various chemokines have been implicated in osteoclastogenesis in vitro, this first systematic analysis of chemokines and receptors during osteoclast differentiation in vivo highlights the key role of CCL9 in this process.

An Interpretation of the Haemocyte Complex in a Stonefly, Acroneuria arenosa Pictet (Plecoptera: Pteronarcidae)

1966 ◽  
Vol 98 (4) ◽  
pp. 394-411 ◽  
Author(s):  
John W. Arnold
Keyword(s):  
Cell Morphology ◽  
Adult Life ◽  
Cell Complex ◽  
The Body ◽  
Progressive Decrease ◽  
Cell Counts ◽  
Wing Veins

AbstractThe haemocytes of adults of the stonefly, Acroneuria arenosa Pictet, are described and figured as they appear in vivo in the wings and as fixed and stained elements in blood films prepared in four different ways. The adequacy of the blood films is judged by comparing the haemocytes there with those in vivo, and the cell complex is interpreted from both aspects. Four categories of haemocytes, the prohaemocytes, plasmatocytes, granular haemocytes, and hyaline haemocytes, are denoted and characterized within these visual limits. The validity of one category, the hyaline haemocytes, is questioned on the basis of cell counts and cell morphology but is tentatively retained. Variations in the haemocyte complex during the adult life is considered. The progressive decrease in relative numbers of circulating plasmatocytes with age is shown to be due to their adherence to the walls of wing veins and presumably to other tissues within the body.

scholarly journals Distribution and Function of Laminins in the Neuromuscular System of Developing, Adult, and Mutant Mice

1997 ◽  
Vol 139 (6) ◽  
pp. 1507-1521 ◽  
Author(s):  
Bruce L. Patton ◽  
Jeffrey H. Miner ◽  
Arlene Y. Chiu ◽  
Joshua R. Sanes
Keyword(s):  
Peripheral Nerve ◽  
Hot Spots ◽  
Muscle Cells ◽  
Synaptic Cleft ◽  
The Body ◽  
Motor Axons ◽  
And Function ◽  
Development Proceeds ◽  
Laminin 1

Laminins, heterotrimers of α, β, and γ chains, are prominent constituents of basal laminae (BLs) throughout the body. Previous studies have shown that laminins affect both myogenesis and synaptogenesis in skeletal muscle. Here we have studied the distribution of the 10 known laminin chains in muscle and peripheral nerve, and assayed the ability of several heterotrimers to affect the outgrowth of motor axons. We show that cultured muscle cells express four different α chains (α1, α2, α4, and α5), and that developing muscles incorporate all four into BLs. The portion of the muscle's BL that occupies the synaptic cleft contains at least three α chains and two β chains, but each is regulated differently. Initially, the α2, α4, α5, and β1 chains are present both extrasynaptically and synaptically, whereas β2 is restricted to synaptic BL from its first appearance. As development proceeds, α2 remains broadly distributed, whereas α4 and α5 are lost from extrasynaptic BL and β1 from synaptic BL. In adults, α4 is restricted to primary synaptic clefts whereas α5 is present in both primary and secondary clefts. Thus, adult extrasynaptic BL is rich in laminin 2 (α2β1γ1), and synaptic BL contains laminins 4 (α2β2γ1), 9 (α4β2γ1), and 11 (α5β2γ1). Likewise, in cultured muscle cells, α2 and β1 are broadly distributed but α5 and β2 are concentrated at acetylcholine receptor–rich “hot spots,” even in the absence of nerves. The endoneurial and perineurial BLs of peripheral nerve also contain distinct laminin chains: α2, β1, γ1, and α4, α5, β2, γ1, respectively. Mutation of the laminin α2 or β2 genes in mice not only leads to loss of the respective chains in both nerve and muscle, but also to coordinate loss and compensatory upregulation of other chains. Notably, loss of β2 from synaptic BL in β2−/− “knockout” mice is accompanied by loss of α5, and decreased levels of α2 in dystrophic α2dy/dy mice are accompanied by compensatory retention of α4. Finally, we show that motor axons respond in distinct ways to different laminin heterotrimers: they grow freely between laminin 1 (α1β1γ1) and laminin 2, fail to cross from laminin 4 to laminin 1, and stop upon contacting laminin 11. The ability of laminin 11 to serve as a stop signal for growing axons explains, in part, axonal behaviors observed at developing and regenerating synapses in vivo.

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