Pathophysiology of Leukocytes System
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WHITE BLOOD CELLS Formation Function ~ TEST YOURSELF
Chapter 9 Blood, Lymph, and Immunity 231 WHITE BLOOD CELLS All white blood cells develop in the bone marrow except Any nucleated cell normally found in blood is a white blood for some lymphocytes (they start out in bone marrow but cell. White blood cells are also known as WBCs or leukocytes. develop elsewhere). At the beginning of leukopoiesis all the When white blood cells accumulate in one place, they grossly immature white blood cells look alike even though they're appear white or cream-colored. For example, pus is an accu- already committed to a specific cell line. It's not until the mulation of white blood cells. Mature white blood cells are cells start developing some of their unique characteristics larger than mature red blood cells. that we can tell them apart. There are five types of white blood cells. They are neu- Function trophils, eosinophils, basophils, monocytes and lymphocytes (Table 9-2). The function of all white blood cells is to provide a defense White blood cells can be classified in three different ways: for the body against foreign invaders. Each type of white 1. Type of defense function blood cell has its own unique role in this defense. If all the • Phagocytosis: neutrophils, eosinophils, basophils, mono- white blood cells are functioning properly, an animal has a cytes good chance of remaining healthy. Individual white blood • Antibody production and cellular immunity: lympho- cell functions will be discussed with each cell type (see cytes Table 9-2). 2. Shape of nucleus In providing defense against foreign invaders, the white • Polymorphonuclear (multilobed, segmented nucleus): blood cells do their jobs primarily out in the tissues. -
• Cytosis: O Neutrophilia: Defined As an Increase in the Neutrophilic Count in the Peripheral Blood Above Reference Range for Age
HENATOLYMPHOID SYSTEM THIRD YEAR MEDICAL STUDENTS-UNIVERSITY OF JORDAN AHMAD T. MANSOUR, MD NONNEOPLASTIC DISEASES OF THE WHITE BLOOD CELLS • There are five major types of WBCs in the blood: neutrophils, lymphocytes, eosinophils, basophils and monocytes. • The normal function of the white blood cells depends on a tight regulation of their count and their function. Therefore, disease develops if there is a derangement of the cells count or function, it takes one of the following forms: o Cytosis: increase in the number of circulating cells above reference range. (Note: leukocytosis means an increase in the WBC count, neutrophilia means increase in the neutrophilic count, lymphocytosis means increase in the lymphocytic count, monocytosis means increase in the monocytic count, basophilia means increase in the basophilic count and eosinophilia means in crease in the eosinophilic count). o Cytopenia: decrease in the number of circulating cells below reference range. (Note: neutropenia means decreased neutrophils, lymphocytopenia, or simply lymphopenia, means decrease in lymphocytes, monocytopenia means decrease in monocytes, eosinopenia means decrease in eosinophils, and basopenia means decrease in basophils). o Abnormal or absent function • Cytosis: o Neutrophilia: defined as an increase in the neutrophilic count in the peripheral blood above reference range for age. o Causes: bacterial infection is the most common and most important etiology. Tissue necrosis in cases of burns or trauma and medications such as epinephrine and corticosteroids are also additional causes for neutrophilia. § Some physiologic conditions can lead to neutrophilia such as stress, smoking and pregnancy. o Pathophysiology: neutrophils are present in the blood in two populations: circulating and marginal (meaning neutrophils stuck to the vessel wall). -
Melanin-Dot–Mediated Delivery of Metallacycle for NIR-II/Photoacoustic Dual-Modal Imaging-Guided Chemo-Photothermal Synergistic Therapy
Melanin-dot–mediated delivery of metallacycle for NIR-II/photoacoustic dual-modal imaging-guided chemo-photothermal synergistic therapy Yue Suna,1, Feng Dingb,1, Zhao Chenb,c,1, Ruiping Zhangd,1, Chonglu Lib, Yuling Xub, Yi Zhangb, Ruidong Nie, Xiaopeng Lie, Guangfu Yangb, Yao Sunb,2, and Peter J. Stangc,2 aKey Laboratory of Catalysis and Material Sciences of the State Ethnic Affairs Commission & Ministry of Education, College of Chemistry and Material Sciences, South-Central University for Nationalities, Wuhan 430074, China; bKey Laboratory of Pesticides and Chemical Biology, Ministry of Education, International Joint Research Center for Intelligent Biosensor Technology and Health, Chemical Biology Center, College of Chemistry, Central China Normal University, Wuhan 430079, China; cDepartment of Chemistry, University of Utah, Salt Lake City, UT 84112; dThe Affiliated Shanxi Da Yi Hospital, Shanxi Academy of Medical Sciences, Taiyuan 020001, China; and eDepartment of Chemistry, University of South Florida, Tampa, FL 33620 Contributed by Peter J. Stang, July 9, 2019 (sent for review May 22, 2019; reviewed by Phil S. Baran and Jean-Marie P. Lehn) Discrete Pt(II) metallacycles have potential applications in bio- compared with traditional methods such as vesicle carriers, mel- medicine. Herein, we engineered a dual-modal imaging and chemo- anin dots can load more drugs through π–π stacking on the high- photothermal therapeutic nano-agent 1 that incorporates discrete volume surface (16, 18). Recent studies reported that melanin Pt(II) metallacycle 2 and fluorescent dye 3 (emission wavelength in dots can absorb near-infrared (NIR) optical energy and convert it the second near-infrared channel [NIR-II]) into multifunctional into heat for photothermal therapy (PTT). -
My Beloved Neutrophil Dr Boxer 2014 Neutropenia Family Conference
The Beloved Neutrophil: Its Function in Health and Disease Stem Cell Multipotent Progenitor Myeloid Lymphoid CMP IL-3, SCF, GM-CSF CLP Committed Progenitor MEP GMP GM-CSF, IL-3, SCF EPO TPO G-CSF M-CSF IL-5 IL-3 SCF RBC Platelet Neutrophil Monocyte/ Basophil B-cells Macrophage Eosinophil T-Cells Mast cell NK cells Mature Cell Dendritic cells PRODUCTION AND KINETICS OF NEUTROPHILS CELLS % CELLS TIME Bone Marrow: Myeloblast 1 7 - 9 Mitotic Promyelocyte 4 Days Myelocyte 16 Maturation/ Metamyelocyte 22 3 – 7 Storage Band 30 Days Seg 21 Vascular: Peripheral Blood Seg 2 6 – 12 hours 3 Marginating Pool Apoptosis and ? Tissue clearance by 0 – 3 macrophages days PHAGOCYTOSIS 1. Mobilization 2. Chemotaxis 3. Recognition (Opsonization) 4. Ingestion 5. Degranulation 6. Peroxidation 7. Killing and Digestion 8. Net formation Adhesion: β 2 Integrins ▪ Heterodimer of a and b chain ▪ Tight adhesion, migration, ingestion, co- stimulation of other PMN responses LFA-1 Mac-1 (CR3) p150,95 a2b2 a CD11a CD11b CD11c CD11d b CD18 CD18 CD18 CD18 Cells All PMN, Dendritic Mac, mono, leukocytes mono/mac, PMN, T cell LGL Ligands ICAMs ICAM-1 C3bi, ICAM-3, C3bi other other Fibrinogen other GRANULOCYTE CHEMOATTRACTANTS Chemoattractants Source Activators Lipids PAF Neutrophils C5a, LPS, FMLP Endothelium LTB4 Neutrophils FMLP, C5a, LPS Chemokines (a) IL-8 Monocytes, endothelium LPS, IL-1, TNF, IL-3 other cells Gro a, b, g Monocytes, endothelium IL-1, TNF other cells NAP-2 Activated platelets Platelet activation Others FMLP Bacteria C5a Activation of complement Other Important Receptors on PMNs ñ Pattern recognition receptors – Detect microbes - Toll receptor family - Mannose receptor - bGlucan receptor – fungal cell walls ñ Cytokine receptors – enhance PMN function - G-CSF, GM-CSF - TNF Receptor ñ Opsonin receptors – trigger phagocytosis - FcgRI, II, III - Complement receptors – ñ Mac1/CR3 (CD11b/CD18) – C3bi ñ CR-1 – C3b, C4b, C3bi, C1q, Mannose binding protein From JG Hirsch, J Exp Med 116:827, 1962, with permission. -
Reprogramming of a Subpopulation of Human Blood Neutrophils By
Laboratory Investigation (2009) 89, 1084–1099 & 2009 USCAP, Inc All rights reserved 0023-6837/09 $32.00 Reprogramming of a subpopulation of human blood neutrophils by prolonged exposure to cytokines Arpita Chakravarti1, Daniel Rusu1, Nicolas Flamand2, Pierre Borgeat1 and Patrice E Poubelle1 Essential cells of innate immunity, neutrophils are often considered to be a homogenous population of terminally differentiated cells. During inflammation, neutrophils are extravasated cells exposed to local factors that prolong their survival and activate their production of mediators implicated in disease progression. In this study, a phenotypically distinct subset of human neutrophils that appear after prolonged exposure to cytokines was characterized. Freshly isolated neutrophils from healthy donors were incubated with granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-a and interleukin (IL)-4, three cytokines that are locally present in various inflammatory conditions. Eight to 17% of neutrophils survived beyond 72 h. This subset of non-apoptotic neutrophils, as evaluated by three different markers, was enriched by discontinuous Percoll gradient centrifugation before studying their phenotype. These viable neutrophils showed neoexpression of HLA-DR, CD80 and CD49d. Compared with freshly isolated neutrophils, they responded differentially to second signals similar to formyl-methionyl-leucyl-phenylalanine with three- to four-fold increases in production of superoxide anions and leukotrienes. These cells augmented their phagocytic index by 141%, increased their adhesion to human primary fibroblasts, but reduced their migration in response to chemotactic stimuli and decreased exocytosis of primary and secondary granules. In addition, they produced substantial amounts of IL-8, IL-1Ra and IL-1b. This neutrophil subset had a unique profile of phosphorylation of intracellular signaling molecules. -
On the Histological Diagnosis and Prognosis of Malignant Melanoma
J Clin Pathol: first published as 10.1136/jcp.33.2.101 on 1 February 1980. Downloaded from J Clin Pathol 1980, 33: 101-124 On the histological diagnosis and prognosis of malignant melanoma ARNOLD LEVENE Hunterian Professor, Royal College of Surgeons, and Department of Histopathology, The Royal Marsden Hospital, Fulham Road, London SW3, UK SUMMARY This review deals with difficulties of diagnosis in cutaneous malignant melanoma encountered by histopathologists of variable seniority and is based on referred material at The Royal Marsden Hospital over a 20-year period and on the experience of more than two-and-a-half thousand cases referred to The World Health Organisation Melanoma Unit which I reviewed when chairman of the Pathologists' Committee. Though there is reference to the differential diagnosis of primary and metastatic tumour, the main concern is with establishing the diagnosis of primary melanoma to the exclusion of all other lesions. An appendix on recommended diagnostic methods in cutaneous melanomas is included. Among the difficult diagnostic fields in histopathol- not to be labelled malignant because it 'looks nasty'. ogy melanocytic tumours have achieved a notoriety. Thus, until the critical evaluation of the 'malignant Accurate diagnosis, however, is of major clinical melanoma of childhood' by Spitz (1948) the naevus importance for the following reasons: with which this investigator's name is associated was 1 The management of the primary lesion is reckoned among the malignancies on histological principally by surgical excision with a large margin grounds. of normal appearing skin. The consequences of over-diagnosis are those of major disfiguring surgery Naevus and melanoma cells http://jcp.bmj.com/ and its morbidity. -
Practice Parameter for the Diagnosis and Management of Primary Immunodeficiency
Practice parameter Practice parameter for the diagnosis and management of primary immunodeficiency Francisco A. Bonilla, MD, PhD, David A. Khan, MD, Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD, David I. Bernstein, MD, Joann Blessing-Moore, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Chief Editor: Francisco A. Bonilla, MD, PhD Co-Editor: David A. Khan, MD Members of the Joint Task Force on Practice Parameters: David I. Bernstein, MD, Joann Blessing-Moore, MD, David Khan, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Primary Immunodeficiency Workgroup: Chairman: Francisco A. Bonilla, MD, PhD Members: Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD GlaxoSmithKline, Merck, and Aerocrine; has received payment for lectures from Genentech/ These parameters were developed by the Joint Task Force on Practice Parameters, representing Novartis, GlaxoSmithKline, and Merck; and has received research support from Genentech/ the American Academy of Allergy, Asthma & Immunology; the American College of Novartis and Merck. -
Infectious Hematopoietic Necrosis in Alaskan Chum Salmon
INFECTIOUS HEMATOPOIETIC NECROSIS IN ALASKAN CHUM SALMON by Roger R. Saft Jill E. Follett Joan Bloom Thomas Number 79 INFECTIOUS HEMATOPOIETIC NECROSIS IN ALASKAN CHUM SALMON Roger R. Saft Jill E. Follett Joan Bloom Thomas Number 79 Alaska Department of Fish and Game Division of Fisheries Rehabilitation, Enhancement and Development Robert D. Burkett, Chief Technology and Development Branch P. 0. Box 3-2000 Juneau, Alaska 99802-2000 November 1987 TABLE OF CONTENTS Section Pase ABSTRACT ............................................ 1 INTRODUCTION .......................................... 1 MATERIALS AND METHODS .................................. 4 Traditional Tissue Culture Assay .................. 4 Plaque-Quantitative Assay ......................... 4 Histopathological Methods ......................... 5 Lab Challenge .............................. 5 RESULTS ............................................ 6 Clinical Signs .................................... 6 Micxoscopic Pathology ............................. 8 Epizootiology ..................................... 13 Lab Challenge ..................................... 14 DISCUSSION .......................................... 16 ACKNOWLEDGMENTS ....................................... 21 REFERENCES ............................................ 22 APPENDIX ............................................... 27 LIST OF TABLES Page 1. Infectious hematopoietic necrosis virus (IHNV) titers (plaque-forming units/gram whole fish tissue*) in mortalities of two chum salmon stocks challenged with two virus -
Myocardial Inflammation, Cellular Death, and Viral Detection In
0031-3998/09/6601-0017 Vol. 66, No. 1, 2009 PEDIATRIC RESEARCH Printed in U.S.A. Copyright © 2009 International Pediatric Research Foundation, Inc. Myocardial Inflammation, Cellular Death, and Viral Detection in Sudden Infant Death Caused by SIDS, Suffocation, or Myocarditis HENRY F. KROUS, CHRISTINE FERANDOS, HOMEYRA MASOUMI, JOHN ARNOLD, ELISABETH A. HAAS, CHRISTINA STANLEY, AND PAUL D. GROSSFELD Departments of Pathology [H.F.K.] and Pediatrics [P.D.G.], University of California, San Diego, LA Jolla, California 92037; Departments of Pathology and Cardiology, Rady Children’s Hospital [H.F.K., C.F., H.M., E.A.H., P.D.G.], San Diego, California 92123; Pediatric Infectious Disease [J.A.], Naval Medical Center San Diego, San Diego, California 92134; San Diego County Medical Examiner Office [C.S.], San Diego, California 92123 ABSTRACT: The significance of minor myocardial inflammatory mechanisms have been proposed to explain the cause(s) of infiltrates and viral detection in SIDS is controversial. We retrospec- death in SIDS. The “triple risk” hypothesis has gained wide- tively compared the demographic profiles, myocardial inflammation, spread acceptance to accommodate the multiple factors now cardiomyocyte necrosis, and myocardial virus detection in infants known to be important in SIDS (5). This states that SIDS who died of SIDS in a safe sleep environment, accidental suffocation, results from the cataclysmic and lethal intersection of the infant’s or myocarditis. Formalin-fixed, paraffin-embedded myocardial sec- tions were semiquantitatively assessed for CD3 lymphocytes and age with its concomitant unstable pathophysiologic status asso- CD68 macrophages using immunohistochemistry and for cardiomy- ciated with an underlying vulnerability while exposed to envi- ocyte cell death in H&E-stained sections. -
Complete Blood Count in Primary Care
Complete Blood Count in Primary Care bpac nz better medicine Editorial Team bpacnz Tony Fraser 10 George Street Professor Murray Tilyard PO Box 6032, Dunedin Clinical Advisory Group phone 03 477 5418 Dr Dave Colquhoun Michele Cray free fax 0800 bpac nz Dr Rosemary Ikram www.bpac.org.nz Dr Peter Jensen Dr Cam Kyle Dr Chris Leathart Dr Lynn McBain Associate Professor Jim Reid Dr David Reith Professor Murray Tilyard Programme Development Team Noni Allison Rachael Clarke Rebecca Didham Terry Ehau Peter Ellison Dr Malcolm Kendall-Smith Dr Anne Marie Tangney Dr Trevor Walker Dr Sharyn Willis Dave Woods Report Development Team Justine Broadley Todd Gillies Lana Johnson Web Gordon Smith Design Michael Crawford Management and Administration Kaye Baldwin Tony Fraser Kyla Letman Professor Murray Tilyard Distribution Zane Lindon Lyn Thomlinson Colleen Witchall All information is intended for use by competent health care professionals and should be utilised in conjunction with © May 2008 pertinent clinical data. Contents Key points/purpose 2 Introduction 2 Background ▪ Haematopoiesis - Cell development 3 ▪ Limitations of reference ranges for the CBC 4 ▪ Borderline abnormal results must be interpreted in clinical context 4 ▪ History and clinical examination 4 White Cells ▪ Neutrophils 5 ▪ Lymphocytes 9 ▪ Monocytes 11 ▪ Basophils 12 ▪ Eosinophils 12 ▪ Platelets 13 Haemoglobin and red cell indices ▪ Low haemoglobin 15 ▪ Microcytic anaemia 15 ▪ Normocytic anaemia 16 ▪ Macrocytic anaemia 17 ▪ High haemoglobin 17 ▪ Other red cell indices 18 Summary Table 19 Glossary 20 This resource is a consensus document, developed with haematology and general practice input. We would like to thank: Dr Liam Fernyhough, Haematologist, Canterbury Health Laboratories Dr Chris Leathart, GP, Christchurch Dr Edward Theakston, Haematologist, Diagnostic Medlab Ltd We would like to acknowledge their advice, expertise and valuable feedback on this document. -
University of Birmingham the Primary Immunodeficiency Disorders
University of Birmingham The primary immunodeficiency disorders Shields, Adrian; Patel, Smita Y DOI: 10.1016/j.mpmed.2017.07.011 License: Creative Commons: Attribution-NonCommercial-NoDerivs (CC BY-NC-ND) Document Version Peer reviewed version Citation for published version (Harvard): Shields, A & Patel, SY 2017, 'The primary immunodeficiency disorders', Medicine, vol. 45, no. 10, pp. 597-604. https://doi.org/10.1016/j.mpmed.2017.07.011 Link to publication on Research at Birmingham portal Publisher Rights Statement: Shields, A. Patel, S. (2017) The primary immunodeficiency disorders, Medicine, volume 45, issue 10, pages 597-604, https://doi.org/10.1016/j.mpmed.2017.07.011 General rights Unless a licence is specified above, all rights (including copyright and moral rights) in this document are retained by the authors and/or the copyright holders. The express permission of the copyright holder must be obtained for any use of this material other than for purposes permitted by law. •Users may freely distribute the URL that is used to identify this publication. •Users may download and/or print one copy of the publication from the University of Birmingham research portal for the purpose of private study or non-commercial research. •User may use extracts from the document in line with the concept of ‘fair dealing’ under the Copyright, Designs and Patents Act 1988 (?) •Users may not further distribute the material nor use it for the purposes of commercial gain. Where a licence is displayed above, please note the terms and conditions of the licence govern your use of this document. When citing, please reference the published version. -
Trapped Neutrophil Syndrome in a Border Collie Dog: Clinical, Clinico-Pathologic, and Molecular Findings
NOTE Internal Medicine Trapped Neutrophil Syndrome in a Border Collie Dog: Clinical, Clinico-Pathologic, and Molecular Findings Keijiro MIZUKAMI1), Tomoaki SHOUBUDANI2), Seira NISHIMOTO2), Ryuta KAWAMURA2), Akira YABUKI1) and Osamu YAMATO1)* 1)Laboratory of Clinical Pathology, Department of Veterinary Medicine, Kagoshima University, 1–21–24 Kohrimoto, Kagoshima 890–0065, Japan 2)Athena Pet Care Clinic, 3 Tamaike-cho, Nishi-ku, Nagoya 452–0812, Japan (Received 21 October 2011/Accepted 27 December 2011/Published online in J-STAGE 12 January 2012) ABSTRACT. Trapped neutrophil syndrome (TNS) is an autosomal recessive inherited neutropenia known in Border Collies since the 1990’s. Recently, the causative mutation has been identified in the canine VPS13B gene and a DNA-based diagnosis has now become available. The present paper describes clinical and clinico-pathologic findings in a Border Collie with TNS that was molecularly diag- nosed for the first time in Japan. In a 10-week-old male Border Collie with microgenesis and symptoms related to recurrent infections, a hematological examination revealed severe leukopenia due to neutropenia, suggesting the dog to be affected by inherited neutro- penic immunodeficiency. Direct DNA sequencing demonstrated that the dog was homozygous for the causative mutation of TNS and both its parents were heterozygous carriers. In addition, a simple and rapid polymerase chain reaction-based length polymorphism analysis coupled with microchip electrophoresis was developed for the genotyping of TNS. This assay could discriminate clearly all genotypes, suggesting that it was suitable for both individual diagnosis and large-scale surveys for prevention. KEY WORDS: Border Collie dog, Cohen syndrome, neutropenia, trapped neutrophil syndrome.