Polymorphonuclear Leucocyte Hypersegmentation in Heat Stroke

Friedman, Ellen; Williams, Jeannine C.; Prendergast, Edward

doi:10.1111/j.1365-2141.1982.tb01901.x

Cited by 8 publications

(3 citation statements)

References 1 publication

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“…In the last decade several reports emphasized nuclear alterations as a special morpho logical feature of certain T-cell lympho mas [Smith et al, 1973;Nathwani et al, 1976;Waldron et al, 1977;Rosen et al, 1978;Pinkus et al, 1979;Said et al, 1979;Lichtenstein et al, 1980;Boucheix et al, 1980;Palutkee t al., 1980;Watanabe et al, 1980;Pallesen et al, 1981;Palacios et al, 1981;Kruskall et al, 1982;Weisenburger et al, 1982], and adult T-cell leukemias [Uchiyama et al, 1977;Hanaoka et al, 1979;McKenna et al, 1979;Costello et al, 1980;Catovskyet al, 1982;Kadin and Kamoun, 1982;Ishiiet al, 1982], Similar fea-tures have only exceptionally been ob served in lymphoproliferative disorders of non-T-cell origin [McKenna et al, 1979]. The nuclear alterations of neoplastic Tcells, among other terms described as 'multilobulated' or 'convoluted', are simi lar to radial segmentation (RS) of leuko cyte nuclei, which is believed to be an in complete amitosis [Neftel and Müller, 1981;Norberg, 1971], RS has been de scribed in hyperthermic states [Hernandez et al, 1980;Friedman et al, 1982], and could be induced in vitro by heat exposure (2 h, 41 °C) in leukocytes of patients with inflammatory and necrotizing disorders, but not in cells of healthy donors [Neftel and Müller, 1981], The first description of radially segmented nuclei, however, was published by Rieder [1893] in a patient with acute leukemia. Since then, illustra tions of 'Rieder cells' are found in many older standard books of hematology.…”

Section: Introductionmentioning

confidence: 99%

Radial Segmentation of Nuclei (Rieder Cells): A Morphological Marker of T-Cell Neoplasms?

Neftel¹,

Stahel²,

Müller³

et al. 1983

Acta Haematol

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Pretreatment blood smears of adult patients with acute lymphoblastic leukemia were examined for neoplastic cells showing nuclear radial segmentation (RS). RS was present in 6 of 7 patients with immunologically proven T-cell leukemia, but not in 11 patients whose leukemic cells lacked T-cell markers. Electron microscopic studies of neoplastic cells showed multiple nuclear indentations and abundant cytoplasmic micro-filaments and microtubuli in connection with pericentriolar dense material. RS formation was decreased in 1 patient after chemotherapy with a vincristine-containing regimen, while the white cell count remained unchanged. Radial segmentation (RS) of leukocyte nuclei is a well-known phenomenon, which is observed ex vivo (Rieder cells), and can be induced in vitro. Convoluted or multilobulated nuclei in lymphoid neoplasms are similar to RS nuclei both with regard to their structure and their sensitivity to spindle-blocking drugs. We propose that the nuclear alterations observed in a variety of different T-cell neoplasms are identical with RS, and suggest that RS might be a morphological marker for subsets of lymphoproliferative disorders of T-cell origin.

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Section: Introductionmentioning

confidence: 99%

Radial Segmentation of Nuclei (Rieder Cells): A Morphological Marker of T-Cell Neoplasms?

Neftel¹,

Stahel²,

Müller³

et al. 1983

Acta Haematol

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“…From tumor-associated neutrophils to professional antigen presenting cells involved in adaptive immunity, to bacterial and parasitic infections and sepsis as well as autoimmune disease, a spectrum of pro-inflammatory, regulatory and suppressive PMNs have been described. Hypersegmented PMN subsets were first noted in the murine tumor microenvironment and more recently have been identified in patients with lung and ovarian cancer, obstructive lung disease, juvenile inflammatory arthritis, hyperthermia, and during experimental endotoxemia (9)(10)(11)(12)(13)(14)(15). Previously thought to occur only in response to in vivo cues, we discovered that infection of human neutrophils with the ulcer and gastric cancer-causing Gram-negative bacterium Helicobacter pylori can induce N1-like subtype differentiation of human neutrophils in vitro that is notable for profound nuclear hypersegmentation, proinflammatory cytokine secretion, a CD62L dim , CD16 bright , CD11b bright , CD66b bright , CD63 bright surface phenotype and a 72 h lifespan (16).…”

Section: Introductionmentioning

confidence: 99%

Microtubules and Dynein Regulate Human Neutrophil Nuclear Volume and Hypersegmentation During H. pylori Infection

Toro

Allen

2021

Front. Immunol.

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Neutrophils (also called polymorphonuclear leukocytes, PMNs) are heterogeneous and can exhibit considerable phenotypic and functional plasticity. In keeping with this, we discovered previously that Helicobacter pylori infection induces N1-like subtype differentiation of human PMNs that is notable for profound nuclear hypersegmentation. Herein, we utilized biochemical approaches and confocal and super-resolution microscopy to gain insight into the underlying molecular mechanisms. Sensitivity to inhibition by nocodazole and taxol indicated that microtubule dynamics were required to induce and sustain hypersegmentation, and super-resolution Stimulated Emission Depletion (STED) imaging demonstrated that microtubules were significantly more abundant and longer in hypersegmented cells. Dynein activity was also required, and enrichment of this motor protein at the nuclear periphery was enhanced following H. pylori infection. In contrast, centrosome splitting did not occur, and lamin B receptor abundance and ER morphology were unchanged. Finally, analysis of STED image stacks using Imaris software revealed that nuclear volume increased markedly prior to the onset of hypersegmentation and that nuclear size was differentially modulated by nocodazole and taxol in the presence and absence of infection. Taken together, our data define a new mechanism of hypersegmentation that is mediated by microtubules and dynein and as such advance understanding of processes that regulate nuclear morphology.

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“…Disturbed immune function also contributes to heat illness and heat fatalities (34). Hypersegmented neutrophils have been described in heat stroke (19) and may provide a diagnostic aid (27).…”

Section: Introductionmentioning

confidence: 99%

Antithrombin and Near‐Fatal Exertional Heat Stroke

et al. 2002

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Heat waves result in excess deaths, excess emergency department visits, and intensive care unit admissions for heat stroke. We describe the clinical features and 3-month outcome of a patient with near-fatal heat stroke, admitted to our intensive care unit in July, 2001. After heavily working for hours at a construction site during a heat wave, the 28-year-old male presented with 41.4 degrees C body temperature and multiorgan failure, consisting of neurological impairment, rhabdomyolysis, acute renal failure, disseminated intravascular coagulation, and acute respiratory distress syndrome (ARDS). In the first week there was no evidence of infection. Treatment included cooling, aggressive volume resuscitation, administration of antithrombin-III concentrates and steroids. The patient survived and recovered normal neurological, renal, respiratory and haematological function, and no disability persisted. This case illustrates survival and complete recovery after multiorgan failure in heat stroke with vigorous intensive care. Treatment with antithrombin and steroids and may well have contributed to the favourable outcome. Correction of reduced antithrombin III levels to supranormal by therapeutic administration of antithrombin III concentrate in disseminated intravascular coagulation of heat stroke was not associated with any bleeding complications.

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Polymorphonuclear Leucocyte Hypersegmentation in Heat Stroke

Cited by 8 publications

References 1 publication

Radial Segmentation of Nuclei (Rieder Cells): A Morphological Marker of T-Cell Neoplasms?

Radial Segmentation of Nuclei (Rieder Cells): A Morphological Marker of T-Cell Neoplasms?

Microtubules and Dynein Regulate Human Neutrophil Nuclear Volume and Hypersegmentation During H. pylori Infection

Antithrombin and Near‐Fatal Exertional Heat Stroke

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